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DENG Lin
Graduate School of Medicine / Center for Infectious Diseases (CID)
Associate Professor

Researcher basic information

■ Research Keyword
  • C型肝炎ウイルス
  • B型肝炎ウイルス
  • ウイルス学
■ Research Areas
  • Life sciences / Virology

Research activity information

■ Award
  • Oct. 2018 一般社団法人神緑会, 第6回神緑会ヤングインベスティゲーターアワード（YIA) 優秀賞, B型肝炎ウイルスXタンパク質の新規結合因子Prdx1とエキソソーム構成因子Exosc5によるHBV RNA分解とHBV増殖制御
    Deng Lin
    Others

  • Oct. 2014 一般社団法人神緑会, 第2回神緑会ヤングインベスティゲーターアワード（YIA) 優秀賞, Ｃ型肝炎ウイルスによるミトコンドリア介在性アポトーシス誘導機構の解明
    Deng Lin
    Others

  • Oct. 2011 社団法人日本肝臓学会, 社団法人日本肝臓学会第10回 MSD Award, Ｃ型肝炎ウイルスによる糖代謝異常の分子機序の解明
    Deng Lin

  • Jun. 2011 社団法人日本肝臓学会, 第４７回日本肝臓学会総会優秀演題賞, Ｃ型肝炎ウイルスは酸化ストレスを介して糖新生を亢進し糖尿病発症に関与する
    Deng Lin

■ Paper
  • Aulia Fitri Rhamadianti, Takayuki Abe, Tomohisa Tanaka, Chikako Ono, Hisashi Katayama, Yoshiteru Makino, Lin Deng, Chieko Matsui, Kohji Moriishi, Fumi Shima, Yoshiharu Matsuura, Ikuo Shoji
    A severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes mild-to-severe respiratory symptoms, including acute respiratory distress. Despite remarkable efforts to investigate the virological and pathological impacts of SARS-CoV-2, many of the characteristics of SARS-CoV-2 infection still remain unknown. The interferon-inducible ubiquitin-like protein ISG15 is covalently conjugated to several viral proteins to suppress their functions. It was reported that SARS-CoV-2 utilizes its papain-like protease (PLpro) to impede ISG15 conjugation, ISGylation. However, the role of ISGylation in SARS-CoV-2 infection remains unclear. We aimed to elucidate the role of ISGylation in SARS-CoV-2 replication. We observed that the SARS-CoV-2 nucleocapsid protein is a target protein for the HERC5 E3 ligase-mediated ISGylation in cultured cells. Site-directed mutagenesis reveals that the residue K374 within the C-terminal spacer B-N3 (SB/N3) domain is required for nucleocapsid-ISGylation, alongside conserved lysine residue in MERS-CoV (K372) and SARS-CoV (K375). We also observed that the nucleocapsid-ISGylation results in the disruption of nucleocapsid oligomerization, thereby inhibiting viral replication. Knockdown of ISG15 mRNA enhanced SARS-CoV-2 replication in the SARS-CoV-2 reporter replicon cells, while exogenous expression of ISGylation components partially hampered SARS-CoV-2 replication. Taken together, these results suggest that SARS-CoV-2 PLpro inhibits ISGylation of the nucleocapsid protein to promote viral replication by evading ISGylation-mediated disruption of the nucleocapsid oligomerization.IMPORTANCEISG15 is an interferon-inducible ubiquitin-like protein that is covalently conjugated to the viral protein via specific Lys residues and suppresses viral functions and viral propagation in many viruses. However, the role of ISGylation in SARS-CoV-2 infection remains largely unclear. Here, we demonstrated that the SARS-CoV-2 nucleocapsid protein is a target protein for the HERC5 E3 ligase-mediated ISGylation. We also found that the residue K374 within the C-terminal spacer B-N3 (SB/N3) domain is required for nucleocapsid-ISGylation. We obtained evidence suggesting that nucleocapsid-ISGylation results in the disruption of nucleocapsid-oligomerization, thereby suppressing SARS-CoV-2 replication. We discovered that SARS-CoV-2 papain-like protease inhibits ISG15 conjugation of nucleocapsid protein via its de-conjugating enzyme activity. The present study may contribute to gaining new insight into the roles of ISGylation-mediated anti-viral function in SARS-CoV-2 infection and may lead to the development of more potent and selective inhibitors targeted to SARS-CoV-2 nucleocapsid protein.
    Sep. 2024, Journal of virology, 98(9) (9), e0085524, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Chie Aoki-Utsubo, Masanori Kameoka, Lin Deng, Muhammad Hanafi, Beti Ernawati Dewi, Pratiwi Sudarmono, Takaji Wakita, Hak Hotta
    Statins, such as lovastatin, have been known to inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Statins were reported to moderately suppress hepatitis C virus (HCV) replication in cultured cells harboring HCV RNA replicons. We report here using an HCV cell culture (HCVcc) system that high concentrations of lovastatin (5-20 μg/mL) markedly enhanced the release of HCV infectious particles (virion) in the culture supernatants by up to 40 times, without enhancing HCV RNA replication, HCV protein synthesis, or HCV virion assembly in the cells. We also found that lovastatin increased the phosphorylation (activation) level of extracellular-signal-regulated kinase 5 (ERK5) in both the infected and uninfected cells in a dose-dependent manner. The lovastatin-mediated increase of HCV virion release was partially reversed by selective ERK5 inhibitors, BIX02189 and XMD8-92, or by ERK5 knockdown using small interfering RNA (siRNA). Moreover, we demonstrated that other cholesterol-lowering statins, but not dehydrolovastatin that is incapable of inhibiting HMG-CoA reductase and activating ERK5, enhanced HCV virion release to the same extent as observed with lovastatin. These results collectively suggest that statins markedly enhance HCV virion release from infected cells through HMG-CoA reductase inhibition and ERK5 activation.
    Jul. 2024, Microbiology and immunology, English, International magazine
    [Refereed]
    Scientific journal

  • Lin Deng, Muchamad Ridotu Solichin, Dewa Nyoman Murti Adyaksa, Maria Alethea Septianastiti, Rhamadianti Aulia Fitri, Gede Ngurah Rsi Suwardan, Chieko Matsui, Takayuki Abe, Ikuo Shoji
    Hepatitis C virus (HCV) is a positive-sense, single-stranded RNA virus that causes chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. The release of infectious HCV particles from infected hepatocytes is a crucial step in viral dissemination and disease progression. While the exact mechanisms of HCV particle release remain poorly understood, emerging evidence suggests that HCV utilizes intracellular membrane trafficking and secretory pathways. These pathways include the Golgi secretory pathway and the endosomal trafficking pathways, such as the recycling endosome pathway and the endosomal sorting complex required for transport (ESCRT)-dependent multivesicular bodies (MVBs) pathway. This review provides an overview of recent advances in understanding the release of infectious HCV particles, with a particular focus on the involvement of the host cell factors that participate in HCV particle release. By summarizing the current knowledge in this area, this review aims to contribute to a better understanding of endosomal pathways involved in the extracellular release of HCV particles and the development of novel antiviral strategies.
    Lead, Dec. 2023, Viruses, 15(12) (12), English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Adi Ariffianto, Lin Deng, Takayuki Abe, Chieko Matsui, Masahiko Ito, Akihide Ryo, Hussein Hassan Aly, Koichi Watashi, Tetsuro Suzuki, Masashi Mizokami, Yoshiharu Matsuura, Ikuo Shoji
    Hepatitis B virus (HBV) infection promotes reactive oxygen species production while paradoxically inducing the expression of antioxidant enzymes. HBV-induced disorders of redox homeostasis are closely associated with the development of hepatic diseases. However, the molecular mechanisms underlying the HBV-induced antioxidant response are poorly understood. The NF-E2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway is an intrinsic defense mechanism against oxidative stress. We here aim to elucidate the role of the Nrf2/ARE signaling pathway in the HBV life cycle. ARE-driven reporter assays revealed that expression of HBV X protein (HBx), but not HBV core, large HBV surface, or HBV polymerase, strongly enhanced ARE-luciferase activity, suggesting that HBx plays an important role in the HBV-induced antioxidant response. Knockdown of Nrf2 resulted in a marked decrease in HBx-induced ARE-luciferase activity. Immunoblot analysis and immunofluorescence staining suggested that HBx activates Nrf2 by increasing Nrf2 protein levels and enhancing Nrf2 nuclear localization. The oxidative stress sensor Kelch-like ECH-associated protein 1 (Keap1) is required for the ubiquitin-dependent degradation of Nrf2. Coimmunoprecipitation analysis revealed that HBx interacted with Keap1, suggesting that HBx competes with Nrf2 for interaction with Keap1. A cell-based ubiquitylation assay showed that HBx promoted polyubiquitylation of Nrf2 via K6-linked polyubiquitin chains, and that this action may be associated with Nrf2 stabilization. A chromatin immunoprecipitation assay suggested that Nrf2 interacts with the HBV core promoter. Overexpression of Nrf2 strongly suppressed HBV core promoter activity, resulting in a marked reduction in viral replication. Based on the above, we propose that Keap1 recognizes HBx to activate the Nrf2/ARE signaling pathway upon HBV infection, thereby inhibiting HBV replication.IMPORTANCEThe Kelch-like ECH-associated protein 1 (Keap1)/NF-E2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway is one of the most important defense mechanisms against oxidative stress. We previously reported that a cellular hydrogen peroxide scavenger protein, peroxiredoxin 1, a target gene of transcription factor Nrf2, acts as a novel HBV X protein (HBx)-interacting protein and negatively regulates hepatitis B virus (HBV) propagation through degradation of HBV RNA. This study further demonstrates that the Nrf2/ARE signaling pathway is activated during HBV infection, eventually leading to the suppression of HBV replication. We provide evidence suggesting that Keap1 interacts with HBx, leading to Nrf2 activation and inhibition of HBV replication via suppression of HBV core promoter activity. This study raises the possibility that activation of the Nrf2/ARE signaling pathway is a potential therapeutic strategy against HBV. Our findings may contribute to an improved understanding of the negative regulation of HBV replication by the antioxidant response.
    Oct. 2023, Journal of virology, 97(10) (10), e0128723, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Juniastuti, Takako Utsumi, Laura Navika Yamani, Zayyin Dinana, Emily Gunawan, Aussie Tahta Maharani, Anisa Lailatul Fitria, Rury M Wahyuni, Soetjipto, Yen Hai Doan, Hiroyuki Shimizu, Koji Ishii, Chieko Matsui, Lin Deng, Takayuki Abe, Kazuhiko Katayama, Maria Inge Lusida, Ikuo Shoji
    Norovirus (NoV) is a leading cause of epidemic and sporadic gastroenteritis in people of all ages. Humans are the primary source of NoV and household contact is one of the risk factors for NoV transmission. However, the mechanisms underlying person-to-person NoV transmission are poorly understood. Here we conducted a survey to profile the frequency and characteristics of intrafamily NoV transmission. Stool samples were collected every week from three households between 2016 and 2020; the total number of samples was 1105. The detection of NoV and the genotyping were performed by reverse transcription-polymerase chain reaction targeting the capsid region and direct sequencing methods. NoV was detected in 3.4% of all samples. Eight NoV genotypes were identified. The most common genotype was GII.17, followed in order by GII.6, GI.6, GII.4, GI.3, and GI.2/GI.8/GI.9. Most NoV-positive samples were obtained from asymptomatic individuals. The highest number of NoV transmissions was found in household 3 (6 infections), followed by household 2 (2 infections), while household 1 had no NoV transmission, suggesting that asymptomatic NoV carriers play a major role in infection as NoV reservoirs in the households. Further clarification of the mode of infection will contribute to improved understanding and an appropriate prevention.
    Oct. 2023, Journal of medical virology, 95(10) (10), e29164, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Transcription Factor JunB Suppresses Hepatitis C Virus Replication.
    Adi Ariffianto, Lin Deng, Saki Harada, Yujiao Liang, Chieko Matsui, Takayuki Abe, Ikuo Shoji
    We previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Activation of JNK contributes to the development of liver diseases, including metabolic disorders, steatosis, liver cirrhosis and hepatocellular carcinoma. JNK is known to have numerous target genes, including JunB, a member of activator protein-1 transcription factor family. However, the roles of JunB in the HCV life cycle and HCV-associated pathogenesis remain unclear. To clarify a physiological role of JunB in HCV infection, we investigated the phosphorylation of JunB in HCV J6/JFH1-infected Huh-7.5 cells. Immunoblot analysis revealed that HCV-induced ROS/JNK activation promoted phosphorylation of JunB. The small interfering RNA (siRNA) knockdown of JunB significantly increased the amount of intracellular HCV RNA as well as the intracellular and extracellular HCV infectivity titers. Conversely, overexpression of JunB significantly reduced the amount of intracellular HCV RNA and the intracellular and extracellular HCV infectivity titers. These results suggest that JunB plays a role in inhibiting HCV propagation. Additionally, HCV-mediated JunB activation promoted hepcidin promoter activity and hepcidin mRNA levels, a key factor in modulating iron homeostasis, suggesting that JunB is involved in HCV-induced transcriptional upregulation of hepcidin. Taken together, we propose that the HCV-induced ROS/JNK/JunB signaling pathway plays roles in inhibiting HCV replication and contributing to HCV-mediated iron metabolism disorder.
    Aug. 2023, The Kobe journal of medical sciences, 69(3) (3), E86-E95, English, Domestic magazine
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Takayuki Abe, Yuki Marutani, Lin Deng, Chieko Matsui, Masayoshi Fukasawa, Ryosuke Suzuki, Takaji Wakita, Yoshiharu Matsuura, Ikuo Shoji
    Annexins (ANXs) comprise a family of calcium- and phospholipid-binding proteins and are implicated in the hepatitis C virus (HCV) life cycle. Here, we demonstrate a novel role of ANX5 in the HCV life cycle. Comparative analysis by quantitative PCR in human hepatoma cells revealed that ANX2, ANX4, and ANX5 were highly expressed among the ANX family proteins. Knockdown of ANX5 mRNA resulted in marked enhancement of HCV RNA replication but had no effect on either HCV translation or assembly. Using the HCV pseudoparticle (HCVpp) system, we observed enhancement of HCVpp infectivity in ANX5 knockdown Huh-7OK1 cells, suggesting that ANX5 is involved in suppression of HCV entry. Additionally, we observed that subcellular localizations of tight-junction proteins, such as claudin 1 (CLDN1) and occludin (OCLN), were disrupted in the ANX5 knockdown cells. It was reported that HCV infection was facilitated by disruption of OCLN distribution and that proper distribution of OCLN was regulated by its phosphorylation. Knockdown of ANX5 resulted in a decrease of OCLN phosphorylation, thereby disrupting OCLN distribution and HCV infection. Further analysis revealed that protein kinase C (PKC) isoforms, including PKCα and PKCη, play important roles in the regulation of ANX5-mediated phosphorylation and distribution of OCLN and in the restriction of HCV infection. HCV infection reduced OCLN phosphorylation through the downregulation of PKCα and PKCη expression. Taken together, these results suggest that ANX5, PKCα, and PKCη contribute to restriction of HCV infection by regulating OCLN integrity. We propose a model that HCV disrupts ANX5-mediated OCLN integrity through downregulation of PKCα and PKCη expression, thereby promoting HCV propagation. IMPORTANCE Host cells have evolved host defense machinery to restrict viral infection. However, viruses have evolved counteracting strategies to achieve their infection. In the present study, we obtained results suggesting that ANX5 and PKC isoforms, including PKCα and PKCη, contribute to suppression of HCV infection by regulating the integrity of OCLN. The disruption of OCLN integrity increased HCV infection. We also found that HCV disrupts ANX5-mediated OCLN integrity through downregulation of PKCα and PKCη expression, thereby promoting viral infection. We propose that HCV disrupts ANX5-mediated OCLN integrity to establish a persistent infection. The disruption of tight-junction assembly may play important roles in the progression of HCV-related liver diseases.
    Jun. 2023, Journal of virology, 97(6) (6), e0065523, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Laura Navika Yamani, Takako Utsumi, Yen Hai Doan, Yoshiki Fujii, Zayyin Dinana, Rury Mega Wahyuni, Emily Gunawan, Soegeng Soegijanto, Alpha Fardah Athiyyah, Subijanto Marto Sudarmo, Reza Gunadi Ranuh, Andy Darma, Soetjipto, Juniastuti, Rheza Gandi Bawono, Chieko Matsui, Lin Deng, Takayuki Abe, Hiroyuki Shimizu, Koji Ishii, Kazuhiko Katayama, Maria Inge Lusida, Ikuo Shoji
    Rotavirus A (RVA) is a major viral cause of acute gastroenteritis worldwide. G12 RVA strains have emerged globally since 2007. There has been no report of the whole genome sequences of G12 RVAs in Indonesia. We performed the complete genome analysis by the next-generation sequencing of five G12 strains from hospitalized children with acute gastroenteritis in Surabaya from 2017-2018. All five G12 strains were Wa-like strains (G12-P[8]-I1-R1-C1-M1-A1-N1-T1-E1-H1) and were clustered into lineage-III of VP7 gene phylogenetic tree. STM430 sample was observed as a mixed-infection between G12 and G1 strains: G12/G1-P[8]-I1-R1-C1-M1-A1-N1-T1-E1-H1. A phylogenetic tree analysis revealed that all five Indonesian G12 strains (SOEP379, STM371, STM413, STM430, and STM433) were genetically close to each other in all 11 genome segments with 98.0-100% nucleotide identities, except VP3 and NSP4 of STM430, suggesting that these strains have originated from a similar ancestral G12 RVA. The VP3 and NSP4 genome segments of STM430-G12P[8] were separated phylogenetically from those of the other four G12 strains, probably due to intra-genotype reassortment between the G12 and G1 Wa-like strains. The change from G12P[6] lineage-II in 2007 to G12P[8] lineage-III 2017-2018 suggests the evolution and diversity of G12 RVAs in Indonesia over the past approximately 10 years. This article is protected by copyright. All rights reserved.
    Jan. 2023, Journal of medical virology, 95(2) (2), e28485, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Putu Yuliandari, Chieko Matsui, Lin Deng, Takayuki Abe, Hiroyuki Mori, Shuhei Taguwa, Chikako Ono, Takasuke Fukuhara, Yoshiharu Matsuura, Ikuo Shoji
    Informa UK Limited, Jul. 2022, Autophagy Reports, 1(1) (1), 264 - 285
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Lin Deng, Yujiao Liang, Adi Ariffianto, Chieko Matsui, Takayuki Abe, Masamichi Muramatsu, Takaji Wakita, Masatoshi Maki, Hideki Shibata, Ikuo Shoji
    We previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. However, the roles of ROS/JNK activation in the HCV life cycle still remain unclear. We sought to identify a novel role of ROS/JNK signaling pathway in the HCV life cycle. Immunoblot analysis revealed that HCV-induced ROS/JNK activation promoted phosphorylation of Itch, a HECT-type E3 ubiquitin ligase, leading to activation of Itch. The siRNA-knockdown of Itch significantly reduced the extracellular HCV infectivity titers, HCV RNA, and HCV core protein without affecting intracellular HCV infectivity titers, HCV RNA, and HCV proteins, suggesting that Itch is involved in release of HCV particles. HCV-mediated JNK/Itch activation specifically promoted polyubiquitylation of an AAA-type ATPase VPS4A, but not VPS4B, required to form multivesicular bodies. Site-directed mutagenesis revealed that two lysine residues (K23 and K121) on VPS4A were important for VPS4A polyubiquitylation. The siRNA-knockdown of VPS4A, but not VPS4B, significantly reduced extracellular HCV infectivity titers. Co-immunoprecipitation analysis revealed that HCV infection specifically enhanced the interaction between CHMP1B, a subunit of endosomal sorting complexes required for transport (ESCRT)-III complex, and VPS4A, but not VPS4B, whereas VPS4A K23R/K121R greatly reduced the interaction with CHMP1B. HCV infection significantly increased ATPase activity of VPS4A, but not VPS4A K23R/K121R or VPS4B, suggesting that HCV-mediated polyubiquitylation of VPS4A contributes to activation of VPS4A. Taken together, we propose that HCV-induced ROS/JNK/Itch signaling pathway promotes VPS4A polyubiquitylation, leading to enhanced VPS4A-CHMP1B interaction and promotion of VPS4A ATPase activity, thereby promoting the release of HCV particles. IMPORTANCE ROS/JNK signaling pathway contributes to liver diseases, including steatosis, metabolic disorders, and hepatocellular carcinoma. We previously reported that HCV activates the ROS/JNK signaling pathway, leading to the enhancement of hepatic gluconeogenesis and apoptosis induction. This study further demonstrates that HCV-induced ROS/JNK signaling pathway activates the E3 ubiquitin ligase Itch to promote release of HCV particles via polyubiquitylation of VPS4A. We provide evidence suggesting that HCV infection promotes the ROS/JNK/Itch signaling pathway and ESCRT/VPS4A machinery to release infectious HCV particles. Our results may lead to a better understanding of the mechanistic details of HCV particle release.
    Lead, Jan. 2022, Journal of virology, 96(6) (6), JVI0181121, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Rheza Gandi Bawono, Takayuki Abe, Mengting Qu, Daisuke Kuroki, Lin Deng, Chieko Matsui, Akihide Ryo, Tetsuro Suzuki, Yoshiharu Matsuura, Masaya Sugiyama, Masashi Mizokami, Kunitada Shimotohno, Ikuo Shoji
    Ubiquitin and ubiquitin-like protein modification play important roles in modulating the functions of viral proteins in many viruses. Here we demonstrate that hepatitis B virus (HBV) X protein (HBx) is modified by ISG15, which is a type I IFN-inducible, ubiquitin-like protein; this modification is called ISGylation. Immunoblot analyses revealed that HBx proteins derived from four different HBV genotypes accepted ISGylation in cultured cells. Site-directed mutagenesis revealed that three lysine residues (K91, K95 and K140) on the HBx protein, which are well conserved among all the HBV genotypes, are involved in acceptance of ISGylation. Using expression plasmids encoding three known E3 ligases involved in the ISGylation to different substrates, we found that HERC5 functions as an E3 ligase for HBx-ISGylation. Treatment with type I and type III IFNs resulted in the limited suppression of HBV replication in Hep38.7-Tet cells. When cells were treated with IFN-α, silencing of ISG15 resulted in a marked reduction of HBV replication in Hep38.7-Tet cells, suggesting a role of ISG15 in the resistance to IFN-α. In contrast, the silencing of USP18 (an ISG15 de-conjugating enzyme) increased the HBV replication in Hep38.7-Tet cells. Taken together, these results suggest that the HERC5-mediated ISGylation of HBx protein confers pro-viral functions on HBV replication and participates in the resistance to IFN-α-mediated antiviral activity.
    Oct. 2021, The Journal of general virology, 102(10) (10), English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • NS5A-ISGylation via Lysine 26 Has a Critical Role for Efficient Propagation of Hepatitis C Virus Genotype 2a.
    Rheza Gandi Bawono, Takayuki Abe, Yasuaki Shibata, Chieko Matsui, Lin Deng, Ikuo Shoji
    We previously reported that hepatitis C virus (HCV) NS5A (1b, Con1) protein accepts covalent ISG15 conjugation at specific lysine (Lys) residues (K44, K68, K166, K215 and K308), exhibiting proviral effects on HCV RNA replication. Here we investigated a role of NS5A-ISGylation via Lys residues in HCV propagation using HCV infectious clone. The alignment of amino acid sequences revealed that 5 Lys residues (K20, K26, K44, K139, and K166) of the 13 Lys residues within NS5A (genotype 2a, JFH1 strain) were conserved compared to those of HCV (genotype 1b, Con1 strain). The cell-based ISGylation assay revealed that the K26 residue in the amphipathic helix (AH) domain and the K139 residue in domain I of NS5A (2a, JFH1) had the potential to accept ISGylation. Use of the HCV replicon carrying luciferase gene revealed that the K26 residue but not K139 residue of NS5A (2a, JFH1) was important for HCV RNA replication. Furthermore, cell culture HCV revealed that the mutation with the K26 residue in combination with K139 or K166 on NS5A (2a, JFH1) resulted in complete abolishment of viral propagation, suggesting that the K26 residue collaborates with either the K139 residue or K166 residue for efficient HCV propagation. Taken together, these results suggest that HCV NS5A protein has the potential to accept ISGylation via specific Lys residues, involving efficient viral propagation in a genotype-specific manner.
    Sep. 2021, The Kobe journal of medical sciences, 67(2) (2), E38-E47, English, Domestic magazine
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Takako Utsumi, Maria Inge Lusida, Zayyin Dinana, Rury Mega Wahyuni, Soegeng Soegijanto, Soetjipto, Alpha Fardah Athiyyah, Subijanto Marto Sudarmo, Reza Gunadi Ranuh, Andy Darma, Juniastuti, Laura Navika Yamani, Yen Hai Doan, Hiroyuki Shimizu, Koji Ishii, Chieko Matsui, Lin Deng, Takayuki Abe, Kazuhiko Katayama, Ikuo Shoji
    Noroviruses are recognized as a leading cause of outbreaks and sporadic cases of acute gastroenteritis (AGE) among individuals of all ages worldwide, especially in children <5 years old. We investigated the epidemiology of noroviruses among hospitalized children at two hospitals in East Java, Indonesia. Stool samples were collected from 966 children with AGE during September 2015-July 2019. All samples were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) for the amplification of both the RNA-dependent RNA polymerase (RdRp) and the capsid genes of noroviruses. The genotypes were determined by phylogenetic analyses. In 2015-2019, noroviruses were detected in 12.3% (119/966) of the samples. Children <2 years old showed a significantly higher prevalence than those ≥2 years old (P = 0.01). NoV infections were observed throughout the year, with the highest prevalence in December. Based on our genetic analyses of RdRp, GII.[P31] (43.7%, 31/71) was the most prevalent RdRp genotype, followed by GII.[P16] (36.6%, 26/71). GII.[P31] was a dominant genotype in 2016 and 2018, whereas GII.[P16] was a dominant genotype in 2015 and 2017. Among the capsid genotypes, the most predominant norovirus genotype from 2015 to 2018 was GII.4 Sydney_2012 (33.6%, 40/119). The most prevalent genotype in each year was GII.13 in 2015, GII.4 Sydney_2012 in 2016 and 2018, and GII.3 in 2017. Based on the genetic analyses of RdRp and capsid sequences, the strains were clustered into 13 RdRp/capsid genotypes; 12 of them were discordant, e.g., GII.4 Sydney[P31], GII.3[P16], and GII.13[P16]. The predominant genotype in each year was GII.13[P16] in 2015, GII.4 Sydney[P31] in 2016, GII.3[P16] in 2017, and GII.4 Sydney[P31] in 2018. Our results demonstrate high detection rates and genetic diversity of norovirus GII genotypes in pediatric AGE samples from Indonesia. These findings strengthen the importance of the continuous molecular surveillance of emerging norovirus strains.
    Elsevier BV, Mar. 2021, Infection, Genetics and Evolution, 88, 104703 - 104703, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Chieko Matsui, Putu Yuliandari, Lin Deng, Takayuki Abe, Ikuo Shoji
    Lysosome incorporate and degrade proteins in a process known as autophagy. There are three types of autophagy; macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Although autophagy is considered a nonselective degradation process, CMA is known as a selective degradation pathway. All proteins internalized in the lysosome via CMA contain a pentapeptide KFERQ-motif, also known as a CMA-targeting motif, which is necessary for selectivity. CMA directly delivers a substrate protein into the lysosome lumen using the cytosolic chaperone HSC70 and the lysosomal receptor LAMP-2A for degradation. Hepatitis C virus (HCV) NS5A protein interacts with hepatocyte-nuclear factor 1α (HNF-1α) together with HSC70 and promotes the lysosomal degradation of HNF-1α via CMA, resulting in HCV-induced pathogenesis. HCV NS5A promotes recruitment of HSC70 to the substrate protein HNF-1α. HCV NS5A plays a crucial role in HCV-induced CMA. Further investigations of HCV NS5A-interacting proteins containing CMA-targeting motifs may help to elucidate HCV-induced pathogenesis.
    2021, Frontiers in cellular and infection microbiology, 11, 796664 - 796664, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Takayuki Abe, Nanae Minami, Rheza Gandi Bawono, Chieko Matsui, Lin Deng, Takasuke Fukuhara, Yoshiharu Matsuura, Ikuo Shoji
    Interferon-stimulated gene 15 (ISG15) is a ubiquitin-like protein that is covalently conjugated to many substrate proteins in order to modulate their functions; this conjugation is called 'ISGylation'. Several groups reported that the ISGylation of hepatitis C virus (HCV) NS5A protein affects HCV replication. However, ISG15 conjugation sites on NS5A are not well determined, and it is unclear whether the role of NS5A-ISGylation in HCV replication is pro-viral or anti-viral. Here we investigated the role of NS5A-ISGylation in HCV replication by using HCV RNA replicons that have a mutation at each lysine (Lys) residue of NS5A protein. Immunoblot analyses revealed that five Lys residues (K44, K68, K166, K215, and K308) of 14 Lys residues within NS5A (1b, Con1) have the potential to accept ISGylation. We tested the NS5A-ISGylation among different HCV genotypes and observed that the NS5A of all of the HCV genotypes accept ISGylation at the multiple Lys residues. Using an HCV luciferase reporter replicon assay revealed that the residue K308 of NS5A is important for HCV (1b, Con1) RNA replication. We observed that K308, one of the Lys residues for NS5A-ISGylation, is located within the binding region of cyclophilin A (CypA), which is the critical host factor for HCV replication. We obtained evidence suggesting that NS5A-ISGylation derived from all of HCV genotypes enhances the interaction between NS5A and CypA. Taken together, these results suggest that NS5A-ISGylation functions as a pro-viral factor and promotes HCV replication via the recruitment of CypA.IMPORTANCEHost cells have evolved host defense machinery (such as innate immunity) to eliminate viral infections. Viruses have evolved several counteracting strategies for achieving an immune escape from host defense machinery, including type-I interferons (IFNs) and inflammatory cytokines. ISG15 is an IFN-inducible, ubiquitin-like protein that is covalently conjugated to the viral protein via specific Lys residues and suppresses viral functions and viral propagation. Here we demonstrate that HCV NS5A protein accepts ISG15-conjugation at specific Lys residues and that the HERC5 E3 ligase specifically promotes NS5A-ISGylation. We obtained evidence suggesting that NS5A-ISGylation facilitates the recruitment of CypA, which is the critical host factor for HCV replication, thereby promoting HCV replication. These findings indicate that E3 ligase HERC5 is a potential therapeutic target for HCV infection. We propose that HCV hijacks an intracellular ISG15 function to escape the host defense machinery in order to establish a persistent infection.
    Jul. 2020, Journal of virology, 94(20) (20), English, International magazine
    [Refereed]
    Scientific journal

  • Deng Lin, Gan X, Ito M, Chen M, Aly HH, Matsui Chieko, Abe Takayuki, Watashi K, Wakita T, Suzuki T, Okamoto T, Matsuura Y, Mizokami M, Shoji Ikuo, Hotta H
    Mar. 2019, J Virol, 93(6) (6), e0220318, English, International magazine
    [Refereed]
    Scientific journal

  • Alpha Fardah Athiyyah, Takako Utsumi, Rury Mega Wahyuni, Zayyin Dinana, Laura Navika Yamani, Soetjipto, Subijanto Marto Sudarmo, Reza Gunadi Ranuh, Andy Darma, Juniastuti, Dadik Raharjo, Chieko Matsui, Lin Deng, Takayuki Abe, Yen Hai Doan, Yoshiki Fujii, Hiroyuki Shimizu, Kazuhiko Katayama, Maria Inge Lusida, Ikuo Shoji
    Group A rotavirus (RVA) is the most important cause of severe gastroenteritis among children worldwide, and effective RVA vaccines have been introduced in many countries. Here we performed a molecular epidemiological analysis of RVA infection among pediatric patients in East Java, Indonesia, during 2015-2018. A total of 432 stool samples were collected from hospitalized pediatric patients with acute gastroenteritis. None of the patients in this cohort had been immunized with an RVA vaccine. The overall prevalence of RVA infection was 31.7% (137/432), and RVA infection was significantly more prevalent in the 6- to 11-month age group than in the other age groups (P < 0.05). Multiplex reverse transcription-PCR (RT-PCR) revealed that the most common G-P combination was equine-like G3P[8] (70.8%), followed by equine-like G3P[6] (12.4%), human G1P[8] (8.8%), G3P[6] (1.5%), and G1P[6] (0.7%). Interestingly, the equine-like strains were exclusively detected until May 2017, but in July 2017 they were completely replaced by a typical human genotype (G1 and G3), suggesting that the dynamic changes in RVA genotypes from equine-like G3 to typical human G1/G3 in Indonesia can occur even in the country with low RVA vaccine coverage rate. The mechanism of the dynamic changes in RVA genotypes needs to be explored. Infants and children with RVA-associated gastroenteritis presented more frequently with some dehydration, vomiting, and watery diarrhea, indicating a greater severity of RVA infection compared to those with non-RVA gastroenteritis. In conclusion, a dynamic change was found in the RVA genotype from equine-like G3 to a typical human genotype. Since severe cases of RVA infection were prevalent, especially in children aged 6 to 11 months or more generally in those less than 2 years old, RVA vaccination should be included in Indonesia's national immunization program.
    2019, Frontiers in microbiology, 10, 940 - 940, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Takako Utsumi, Rury Mega Wahyuni, Yen Hai Doan, Zayyin Dinana, Soegeng Soegijanto, Yoshiki Fujii, Juniastuti, Laura Navika Yamani, Chieko Matsui, Lin Deng, Takayuki Abe, Soetjipto, Maria Inge Lusida, Koji Ishii, Hiroyuki Shimizu, Kazuhiko Katayama, Ikuo Shoji
    Rotavirus A (RVA) is a major cause of acute gastroenteritis in humans and animals worldwide. As a result of the segmented nature of the rotavirus genome, genetic reassortment commonly occurs. This study aims to clarify the genetic characteristics of RVAs circulating in Indonesia. From June 2015 through August 2016, stool samples were collected from 134 children aged <5 years (71 male and 63 female) with acute gastroenteritis who were inpatients at a private hospital in Surabaya, Indonesia. All stool samples were screened for RVA antigen using immunochromatography. Forty-two samples (31.3%, 42/134) were RVA antigen-positive. All RVA positive samples tested showed the unusual combinations of G3P[8] (n = 36) and G3P[6] (n = 3) with a short RNA pattern by G/P typing and polyacrylamide gel electrophoresis (PAGE). Whole genome analysis by next-generation sequencing (NGS) was performed for 11 strains to determine the RVA genotypes. Eleven rotavirus strains were found to carry a DS-like genetic backbone; nine strains showed a G3-P[8]-I2-R2-C2-M2-A2-N2-T2-E2-H2 genome constellation, which was recently reported in Australia, Hungary, Spain and Brazil; as well, two strains showed a G3-P[6]-I2-R2-C2-M2-A2-N2-T2-E2-H2 genome constellation. The phylogenetic tree based on the VP7 gene showed that all 11 strains were classified as equine-like G3, which is genetically distinct and different in origin from typical human G3 strains. The phylogenetic tree based on the NSP4 gene showed that six strains were classified as bovine-like strain and the remaining five were classified as human strain. In conclusion, we identified the strains which are intergenogroup reassortants containing an equine-like G3 VP7, a P[8])/P[6] VP4, with a DS-1-like genetic backbone. These findings suggest that equine-like G3P[8] and P[6] RVA strains have been circulating in the Indonesian population for at least 1 year and probably longer, indicating a diversity of RVAs in this area.
    Jul. 2018, Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 61(1) (1), 224 - 228, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Matsui Chieko, Deng Lin, Minami N, Abe Takayuki, Koike K, Shoji Ikuo
    Hepatitis C virus (HCV) infection is closely associated with type 2 diabetes. We reported that HCV infection induces the lysosomal degradation of hepatocyte nuclear factor 1 alpha (HNF-1α) via interaction with HCV nonstructural protein 5A (NS5A) protein, thereby suppressing GLUT2 gene expression. The molecular mechanisms of selective degradation of HNF-1α caused by NS5A are largely unknown. Chaperone-mediated autophagy (CMA) is a selective lysosomal degradation pathway. Here, we investigated whether CMA is involved in the selective degradation of HNF-1α in HCV-infected cells and observed that the pentapeptide spanning from amino acid (aa) 130 to aa 134 of HNF-1α matches the rule for the CMA-targeting motif, also known as KFERQ motif. A cytosolic chaperone protein, heat shock cognate protein of 70 kDa (HSC70), and a lysosomal membrane protein, lysosome-associated membrane protein type 2A (LAMP-2A), are key components of CMA. Immunoprecipitation analysis revealed that HNF-1α was coimmunoprecipitated with HSC70, whereas the Q130A mutation (mutation of Q to A at position 130) of HNF-1α disrupted the interaction with HSC70, indicating that the CMA-targeting motif of HNF-1α is important for the association with HSC70. Immunoprecipitation analysis revealed that increasing amounts of NS5A enhanced the association of HNF-1α with HSC70. To determine whether LAMP-2A plays a role in the degradation of HNF-1α protein, we knocked down LAMP-2A mRNA by RNA interference; this knockdown by small interfering RNA (siRNA) recovered the level of HNF-1α protein in HCV J6/JFH1-infected cells. This result suggests that LAMP-2A is required for the degradation of HNF-1α. Immunofluorescence study revealed colocalization of NS5A and HNF-1α in the lysosome. Based on our findings, we propose that HCV NS5A interacts with HSC70 and recruits HSC70 to HNF-1α, thereby promoting the lysosomal degradation of HNF-1α via CMA.IMPORTANCE Many viruses use a protein degradation system, such as the ubiquitin-proteasome pathway or the autophagy pathway, for facilitating viral propagation and viral pathogenesis. We investigated the mechanistic details of the selective lysosomal degradation of hepatocyte nuclear factor 1 alpha (HNF-1α) induced by hepatitis C virus (HCV) NS5A protein. Using site-directed mutagenesis, we demonstrated that HNF-1α contains a pentapeptide chaperone-mediated autophagy (CMA)-targeting motif within the POU-specific domain of HNF-1α. The CMA-targeting motif is important for the association with HSC70. LAMP-2A is required for degradation of HNF-1α caused by NS5A. We propose that HCV NS5A interacts with HSC70, a key component of the CMA machinery, and recruits HSC70 to HNF-1α to target HNF-1α for CMA-mediated lysosomal degradation, thereby facilitating HCV pathogenesis. We discovered a role of HCV NS5A in CMA-dependent degradation of HNF-1α. Our results may lead to a better understanding of the role of CMA in the pathogenesis of HCV.
    Jun. 2018, J Virol, 92(13) (13), e0063918, English, International magazine
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • 脱ユビキチン化酵素USP15阻害剤候補分子の機能解析
    勝二 郁夫, 松井 千絵子, Deng Lin, 阿部 隆之
    生命科学系学会合同年次大会運営事務局, Dec. 2017, 生命科学系学会合同年次大会, 2017年度, [3LBA - 019], Japanese

  • Takako Utsumi, Maria Inge Lusida, Zayyin Dinana, Rury Mega Wahyuni, Laura Navika Yamani, Juniastuti, Soetjipto, Chieko Matsui, Lin Deng, Takayuki Abe, Yen Hai Doan, Yoshiki Fujii, Hirokazu Kimura, Kazuhiko Katayama, Ikuo Shoji
    Nov. 2017, INFECTION GENETICS AND EVOLUTION, 55, 1 - 7, English
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Ming Chen, Chie Aoki-Utsubo, Masanori Kameoka, Lin Deng, Yutaka Terada, Wataru Kamitani, Kei Sato, Yoshio Koyanagi, Makoto Hijikata, Keiko Shindo, Takeshi Noda, Michinori Kohara, Hak Hotta
    Nov. 2017, SCIENTIFIC REPORTS, 7(1) (1), 15931, English
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Nanae Minami, Takayuki Abe, Lin Deng, Chieko Matsui, Takasuke Fukuhara, Yoshiharu Matsuura, Ikuo Shoji
    Jul. 2017, MICROBIOLOGY AND IMMUNOLOGY, 61(7) (7), 287 - 292, English
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Ming Chen, Xiang Gan, Ken-ichi Yoshino, Madoka Kitakawa, Ikuo Shoji, Lin Deng, Hak Hotta
    Corresponding, Jun. 2016, MICROBIOLOGY AND IMMUNOLOGY, 60(6) (6), 407 - 417, English
    [Refereed]
    Scientific journal

  • Miwako Hayashi, Lin Deng, Ming Chen, Xiang Gan, Kenta Shinozaki, Ikuo Shoji, Hak Hotta
    Corresponding, Jan. 2016, MICROBIOLOGY AND IMMUNOLOGY, 60(1) (1), 17 - 25, English
    [Refereed]
    Scientific journal

  • 脱ユビキチン化酵素USP15阻害剤の探索
    勝二 郁夫, Sianipar Imelda Rosalyn, 南 奈苗, 陳 明, 松井 千絵子, Lin Deng
    (公社)日本生化学会, Dec. 2015, 日本生化学会大会・日本分子生物学会年会合同大会講演要旨集, 88回・38回, [1P0487] - [1P0487], Japanese

  • Lin Deng, Ming Chen, Motofumi Tanaka, Yonson Ku, Tomoo Itoh, Ikuo Shoji, Hak Hotta
    Sep. 2015, JOURNAL OF GENERAL VIROLOGY, 96(9) (9), 2670 - 2683, English
    [Refereed]
    Scientific journal

  • Imelda Rosalyn Sianipar, Chieko Matsui, Nanae Minami, Xiang Gan, Lin Deng, Hak Hotta, Ikuo Shoji
    Aug. 2015, MICROBIOLOGY AND IMMUNOLOGY, 59(8) (8), 466 - 476, English
    [Refereed]
    Scientific journal

  • Chieko Matsui, Imelda Rosalyn Sianipar, Nanae Minami, Lin Deng, Hak Hotta, Ikuo Shoji
    Aug. 2015, JOURNAL OF GENERAL VIROLOGY, 96(8) (8), 2200 - 2205, English
    [Refereed]
    Scientific journal

  • Alaa M. H. El-Bitar, Moustafa M. H. Sarhan, Chie Aoki, Yusuke Takahara, Mari Komoto, Lin Deng, Mohsen A. Moustafa, Hak Hotta
    Mar. 2015, VIROLOGY JOURNAL, 12, 47, English
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • [Hepatitis C virus-induced glucose metabolic disorder].
    Ikuo Shoji, Lin Deng, Chieko Matsui, Hak Hotta
    Hepatitis C virus (HCV) infection often causes intrahepatic diseases, such as chronic hepatitis, liver chirrohsis, and hepatocellular carcinoma (HCC). Moreover, HCV infection exhibits various extrahepatic manifestations, such as thyroiditis, glucose and lipid metabolic disorder, and iron metabolic disorder. HCV infection is often associated with type 2 diabetes, involving hepatic fibrosis and poor prognosis. Type 2 diabetes increases the risk of HCC. We have been investigating molecular mechanisms of HCV-induced glucose metabolic disorder and we reported that HCV infection promotes hepatic gluconeogenesis through forkhead box O1 (FoxO1)-dependent pathway and that HCV infection suppresses the cell surface expression of glucose transporter 2 (GLUT2), resulting in suppression of glucose uptake. We have found that HCV NS5A protein plays important roles in these two independent pathways. Here we discuss the roles of HCV NS5A in HCV-induced glucose metabolic disorder.
    2015, Uirusu, 65(2) (2), 263 - 268, Japanese, Domestic magazine
    Scientific journal

  • Jude Juventus Aweya, Ching Wooen Sze, Anthony Bayega, Nur Khairiah Mohd-Ismail, Lin Deng, Hak Hotta, Yee-Joo Tan
    Jan. 2015, VIROLOGY, 474, 41 - 51, English
    [Refereed]
    Scientific journal

  • The NS5A protein of hepatitis C virus transcriptionally upregulates the AGR3 gene expression
    Ming Chen, Xiang Gan, Lin Deng, Hak Hotta
    Kobe University School of Medicine, 2015, Kobe Journal of Medical Sciences, 61(1) (1), E27 - E35, English
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Suratno Lulut Ratnoglik, Da-Peng Jiang, Chie Aoki, Pratiwi Sudarmono, Ikuo Shoji, Lin Deng, Hak Hotta
    Jun. 2014, PLOS ONE, 9(6) (6), e98877, English
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Suratno Lulut Ratnoglik, Chie Aoki, Pratiwi Sudarmono, Mari Komoto, Lin Deng, Ikuo Shoji, Hiroyuki Fuchino, Nobuo Kawahara, Hak Hotta
    Mar. 2014, MICROBIOLOGY AND IMMUNOLOGY, 58(3) (3), 188 - 194, English
    [Refereed]
    Scientific journal

  • Myrna Adianti, Chie Aoki, Mari Komoto, Lin Deng, Ikuo Shoji, Tutik Sri Wahyuni, Maria Inge Lusida, Soetjipto, Hiroyuki Fuchino, Nobuo Kawahara, Hak Hotta
    Mar. 2014, MICROBIOLOGY AND IMMUNOLOGY, 58(3) (3), 180 - 187, English
    [Refereed]
    Scientific journal

  • Ahmed El-Shamy, Michiko Shindo, Ikuo Shoji, Lin Deng, Tadao Okuno, Hak Hotta
    Aug. 2013, Hepatology, 58(2) (2), 555 - 563, English
    [Refereed]
    Scientific journal

  • Tutik Sri Wahyuni, Lydia Tumewu, Adita Ayu Permanasari, Evhy Apriani, Myrna Adianti, Abdul Rahman, Aty Widyawaruyanti, Maria Inge Lusida, Achmad Fuad, Soetjipto, Nasronudin, Hiroyuki Fuchino, Nobuo Kawahara, Ikuo Shoji, Lin Deng, Chie Aoki, Hak Hotta
    Aug. 2013, VIROLOGY JOURNAL, 10(1) (1), 259, English
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Ahmed El-Shamy, Ikuo Shoji, Wafaa El-Akel, Shymaa E. Bilasy, Lin Deng, Maissa El-Raziky, Da-peng Jiang, Gamal Esmat, Hak Hotta
    Dec. 2012, JOURNAL OF CLINICAL MICROBIOLOGY, 50(12) (12), 3886 - 3892, English
    [Refereed]
    Scientific journal

  • Chieko Matsui, Ikuo Shoji, Shusaku Kaneda, Imelda Rosalyn Sianipar, Lin Deng, Hak Hotta
    Dec. 2012, JOURNAL OF VIROLOGY, 86(23) (23), 12903 - 12911, English
    [Refereed]
    Scientific journal

  • Kenji Nakashima, Kenji Takeuchi, Kazuyasu Chihara, Tomoko Horiguchi, Xuedong Sun, Lin Deng, Ikuo Shoji, Hak Hotta, Kiyonao Sada
    Oct. 2012, PLOS ONE, 7(10) (10), English
    [Refereed]
    Scientific journal

  • Soo Ryang Kim, Ahmed El-Shamy, Susumu Imoto, Ke Ih Kim, Yoshi-hiro Ide, Lin Deng, Ikuo Shoji, Yasuhito Tanaka, Yutaka Hasegawa, Mitsuhiro Ota, Hak Hotta
    Oct. 2012, JOURNAL OF GASTROENTEROLOGY, 47(10) (10), 1143 - 1151, English
    [Refereed]
    Scientific journal

  • HCV NS5A protein containing potential ligands for both Src homology 2 and 3 domains enhances autophosphorylation of Src family kinase Fyn in B cells
    K. Sada, K. Nakashima, K. Takeuchi, K. Chihara, T. Horiguchi, L. Deng, I. Shoji, H. Hotta
    Sep. 2012, FEBS JOURNAL, 279(10) (10), 161 - 162, English
    [Refereed]
    Scientific journal

  • Ahmed El-Shamy, Ikuo Shoji, Soo-Ryang Kim, Yoshihiro Ide, Susumu Imoto, Lin Deng, Seitetsu Yoon, Takashi Fujisawa, Satoshi Tani, Yoshihiko Yano, Yasushi Seo, Takeshi Azuma, Hak Hotta
    Feb. 2012, PLOS ONE, 7(2) (2), English
    [Refereed]
    Scientific journal

  • Mikiko Sasayama, Ikuo Shoji, Myrna Adianti, Da-Peng Jiang, Lin Deng, Takafumi Saito, Hisayoshi Watanabe, Sumio Kawata, Chie Aoki, Hak Hotta
    Feb. 2012, JOURNAL OF MEDICAL VIROLOGY, 84(2) (2), 229 - 234, English
    [Refereed]
    Scientific journal

  • Kazuya Kamada, Ikuo Shoji, Lin Deng, Chie Aoki, Suratno Lulut Ratnoglik, Takaji Wakita, Hak Hotta
    Jan. 2012, MICROBES AND INFECTION, 14(1) (1), 69 - 78, English
    [Refereed]
    Scientific journal

  • Ahmed El-Shamy, Soo-Ryang Kim, Yoshi-Hiro Ide, Noriko Sasase, Susumu Imoto, Lin Deng, Ikuo Shoji, Hak Hotta
    2012, INTERVIROLOGY, 55(1) (1), 1 - 11, English
    [Refereed]
    Scientific journal

  • Lin Deng, Ikuo Shoji, Wataru Ogawa, Shusaku Kaneda, Tomoyoshi Soga, Da-peng Jiang, Yoshi-Hiro Ide, Hak Hotta
    Lead, Sep. 2011, JOURNAL OF VIROLOGY, 85(17) (17), 8556 - 8568, English
    [Refereed]
    Scientific journal

  • Ahmed El-Shamy, Ikuo Shoji, Takafumi Saito, Hisayoshi Watanabe, Yoshi-Hiro Ide, Lin Deng, Sumio Kawata, Hak Hotta
    Jun. 2011, Microbiology and Immunology, 55(6) (6), 418 - 426, English
    [Refereed]
    Scientific journal

  • Kazumi Hayashida, Ikuo Shoji, Lin Deng, Da-Peng Jiang, Yoshi-Hiro Ide, Hak Hotta
    Nov. 2010, MICROBIOLOGY AND IMMUNOLOGY, 54(11) (11), 684 - 690, English
    [Refereed]
    Scientific journal

  • Mai Sanjo, Takafumi Saito, Rika Ishii, Yuko Nishise, Hiroaki Haga, Kazuo Okumoto, Junitsu Ito, Hisayoshi Watanabe, Koji Saito, Hitoshi Togashi, Kazuto Fukuda, Yasuharu Imai, Ahmed El-Shamy, Lin Deng, Ikuo Shoji, Hak Hotta, Sumio Kawata
    Aug. 2010, JOURNAL OF MEDICAL VIROLOGY, 82(8) (8), 1364 - 1370, English
    [Refereed]
    Scientific journal

  • Analysis of neutralizing antibodies against hepatitis C virus in patients who were treated with pegylated-interferon plus ribavirin
    Mikiko Sasayama, Lin Deng, Soo Ryang Kim, Yoshi-Hiro Ide, Ikuo Shoji, Hak Hotta
    2010, Kobe Journal of Medical Sciences, 56(2) (2), E60 - E66, English
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Nur Khairiah Mohd-Ismail, Lin Deng, Sunil Kumar Sukumaran, Victor C. Yu, Hak Hotta, Yee-Joo Tan
    Oct. 2009, JOURNAL OF VIROLOGY, 83(19) (19), 9993 - 10006, English
    [Refereed]
    Scientific journal

  • Yasuaki Bungyoku, Ikuo Shoji, Tatsuhiko Makine, Tetsuya Adachi, Kazumi Hayashida, Motoko Nagano-Fujii, Yoshi-Hiro Ide, Lin Deng, Hak Hotta
    Jul. 2009, JOURNAL OF GENERAL VIROLOGY, 90, 1681 - 1691, English
    [Refereed]
    Scientific journal

  • Daisuke Kasai, Tetsuya Adachi, Lin Deng, Motoko Nagano-Fujii, Kiyonao Sada, Masanori Ikeda, Nobuyuki Kato, Yoshi-Hiro Ide, Ikuo Shoji, Hak Hotta
    May 2009, JOURNAL OF HEPATOLOGY, 50(5) (5), 883 - 894, English
    [Refereed]
    Scientific journal

  • Lin Deng, Tetsuya Adachi, Kikumi Kitayama, Yasuaki Bungyoku, Sohei Kitazawa, Satoshi Ishido, Ikuo Shoji, Hak Hotta
    Lead, Nov. 2008, JOURNAL OF VIROLOGY, 82(21) (21), 10375 - 10385, English
    [Refereed]
    Scientific journal

  • Y Nomura-Takigawa, M Nagano-Fujii, L Deng, S Kitazawa, S Ishido, K Sada, H Hotta
    Jul. 2006, JOURNAL OF GENERAL VIROLOGY, 87(Pt 7) (Pt 7), 1935 - 1945, English
    [Refereed]
    Scientific journal

  • L Deng, M Nagano-Fujii, M Tanaka, Y Nomura-Takigawa, M Ikeda, N Kato, K Sada, H Hotta
    Lead, Jun. 2006, JOURNAL OF GENERAL VIROLOGY, 87, 1703 - 1713, English
    [Refereed]
    Scientific journal

  • M Tanaka, M Nagano-Fujii, L Deng, S Ishido, K Sada, H Hotta
    Feb. 2006, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 340(3) (3), 792 - 799, English
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • R Hidajat, M Nagano-Fujii, L Deng, M Tanaka, Y Takigawa, S Kitazawa, H Hotta
    Aug. 2005, JOURNAL OF GENERAL VIROLOGY, 86(8) (8), 2197 - 2208, English
    [Refereed]
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Nonstructural proteins 4A and 4B of hepatitis C virus transactivate the interleukin 8 promoter
    H Kadoya, M Nagano-Fujii, L Deng, N Nakazono, H Hotta
    2005, MICROBIOLOGY AND IMMUNOLOGY, 49(3) (3), 265 - 273, English
    [Refereed]
    Scientific journal

  • Suppression of hepatitis C virus replicon by RNA interference directed against the NS3 and NS5B regions of the viral genome
    Y Takigawa, M Nagano-Fujii, L Deng, R Hidajat, M Tanaka, H Mizuta, H Hotta
    2004, MICROBIOLOGY AND IMMUNOLOGY, 48(8) (8), 591 - 598, English
    [Refereed]
    Scientific journal

  • Cleavage of the hepatitis C virus NS5A protein by caspase-3 in the interferon sensitivity-determining region in a sequence-dependent manner
    Rachmat Hidajat, Motoko Nagano-Fujii, Lin Deng, Hak Hotta
    2004, Kobe Journal of Medical Sciences, 50(5) (5), 153 - 166, English
    [Refereed]
    Scientific journal

  • S Ogata, RH Florese, M Nagano-Fujii, R Hidajat, L Deng, Y Ku, S Yoon, T Saito, S Kawata, H Hotta
    Jul. 2003, JOURNAL OF CLINICAL MICROBIOLOGY, 41(7) (7), 2835 - 2841, English
    Scientific journal
    Link to Kobe Univ. Repository (Kernel)

  • Hepatitis C virus core protein selectively inhibits synthesis and accumulation of p21/Waf1 and certain nuclear proteins
    K Oka, M Nagano-Fujii, Yoshida, I, R Hidajat, L Deng, M Akutsu, H Hotta
    2003, MICROBIOLOGY AND IMMUNOLOGY, 47(6) (6), 429 - 438, English
    [Refereed]
    Scientific journal

  • Physical interaction between hepatitis C virus NS4B protein and CREB-RP/ATF6 beta
    WY Tong, M Nagano-Fujii, R Hidajat, L Deng, Y Takigawa, H Hotta
    Dec. 2002, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 299(3) (3), 366 - 372, English
    [Refereed]
    Scientific journal

■ MISC
  • Unusual G9P[4] rotavirus emerged after the dynamic changes in rotavirus genotypes from equine-like G3 to typical human G1/G3 in Indonesia
    DINANA Zayyin, DINANA Zayyin, DOAN Yen Hai, MAHARANI Aussie Tahta, FITRIA Anisa Lailatul, YAMANI Laura Navika, YAMANI Laura Navika, JUNIASTUTI Juniastuti, SOETJIPTO Soetjipto, SOETJIPTO Soetjipto, MATSUI Chieko, DENG Lin, ABE Takayuki, TAKEMAE Nobuhiro, KAGEYAMA Tsutomu, KATAYAMA Kazuhiko, LUSIDA Maria Inge, LUSIDA Maria Inge, SHOJI Ikuo
    2023, 日本ウイルス学会学術集会プログラム・予稿集(Web), 70th

  • 細胞内アネキシン5はC型肝炎ウイルスの増殖抑制に関与する
    阿部隆之, 松井千絵子, DENG Lin, 松浦善治, 勝二郁夫
    2020, 日本分子生物学会年会プログラム・要旨集(Web), 43rd

  • HCV NS3/4AプロテアーゼはSPG20を選択的に切断し脂肪滴の巨大化を促進する
    松井千絵子, YULIANDARI Putu, DENG Lin, 阿部隆之, 勝二郁夫
    2020, 日本分子生物学会年会プログラム・要旨集(Web), 43rd

  • HCV NS3/4AプロテアーゼはSPG20を選択的に切断し脂肪滴の巨大化を促進する
    松井千絵子, PUTU Yuliandari, LIN Deng, 阿部隆之, 勝二郁夫
    2019, 日本ウイルス学会学術集会プログラム・予稿集(Web), 67th

  • C型肝炎ウイルスNS5A蛋白質のISGylation修飾反応におけるウイルス遺伝子型間の解析
    阿部隆之, 松井千絵子, LIN Deng, 福原崇介, 松浦善治, 勝二郁夫
    2019, 日本ウイルス学会学術集会プログラム・予稿集(Web), 67th

  • 脱ユビキチン化酵素USP15阻害剤候補分子の機能解析
    勝二郁夫, 松井千絵子, DENG Lin, 阿部隆之
    2017, 日本生化学会大会(Web), 90th

  • 脱ユビキチン化酵素USP15阻害剤の探索と機能解析
    勝二郁夫, DENG Lin, 松井千絵子, 南奈苗, 阿部隆之
    2016, 日本分子生物学会年会プログラム・要旨集(Web), 39th

  • 勝二 郁夫, 鄧 琳, 松井 千絵子, HOTTA HAK
    Hepatitis C virus (HCV) infection often causes intrahepatic diseases, such as chronic hepatitis, liver chirrohsis, and hepatocellular carcinoma (HCC). Moreover, HCV infection exhibits various extrahepatic manifestations, such as thyroiditis, glucose and lipid metabolic disorder, and iron metabolic disorder. HCV infection is often associated with type 2 diabetes, involving hepatic fibrosis and poor prognosis. Type 2 diabetes increases the risk of HCC. We have been investigating molecular mechanisms of HCV-induced glucose metabolic disorder and we reported that HCV infection promotes hepatic gluconeogenesis through forkhead box O1 (FoxO1)-dependent pathway and that HCV infection suppresses the cell surface expression of glucose transporter 2 (GLUT2), resulting in suppression of glucose uptake. We have found that HCV NS5A protein plays important roles in these two independent pathways. Here we discuss the roles of HCV NS5A in HCV-induced glucose metabolic disorder.
    The Japanese Society for Virology, Dec. 2015, ウイルス, 65(2) (2), 263 - 268, Japanese
    [Refereed][Invited]
    Introduction scientific journal

  • C型肝炎ウイルス感染によるHepatocyte nuclear factor(HNF)-1α蛋白質の選択的分解機構
    松井千絵子, 勝二郁夫, SIANIPAR Imelda Rosalyn, 南奈苗, DENG Lin, 堀田博
    2014, 日本ウイルス学会学術集会プログラム・抄録集, 62nd

  • C型肝炎ウイルスによるHNF-1α蛋白質の選択的分解機構の解析
    勝二郁夫, 松井千絵子, SIANIPAR Imelda Rosalyn, 南奈苗, DENG Lin, 堀田博
    2014, 日本分子生物学会年会プログラム・要旨集(Web), 37th

  • HCV NS5AとHepatocyte nuclear factor(HNF)-1αの相互作用と病態生理
    松井千絵子, 勝二郁夫, 南奈苗, SIANIPAR Imelda Rosalyn, DENG Lin, 堀田博
    2013, 日本ウイルス学会学術集会プログラム・抄録集, 61st

  • HCV感染による糖代謝障害の分子機序
    勝二郁夫, 松井千絵子, LIN Deng, 堀田博
    2013, 日本ウイルス学会学術集会プログラム・抄録集, 61st

  • C型肝炎ウイルスNS5AはB細胞のチロシンキナーゼFynを活性化する
    中島謙治, 竹内健二, 千原一泰, 堀口朋子, 孫雪東, DENG Lin, 勝二郁夫, 堀田博, 定清直
    31 Oct. 2012, 日本ウイルス学会学術集会プログラム・抄録集, 60th, 244, Japanese

  • C型肝炎ウイルスによるGLUT2遺伝子発現抑制の分子機構
    松井千絵子, 勝二郁夫, DENG Lin, 堀田博
    2012, 日本ウイルス学会学術集会プログラム・抄録集, 60th

  • C型肝炎ウイルス感染はHNF-1αの発現を負に制御しGLUT2遺伝子発現を抑制する
    勝二郁夫, 松井千絵子, 兼田祟作, IMELDA Rosalyn Sianipar, DENG Lin, 堀田博
    2012, 日本分子生物学会年会プログラム・要旨集(Web), 35th

  • C型肝炎ウイルスNS5A蛋白質のSrc homology2/3ドメイン結合能とB細胞での発現によるSrcファミリーキナーゼFynの活性化
    中島謙治, 竹内健司, 千原一泰, 堀口朋子, SUN Xuedong, LIN Deng, 勝二郁夫, 堀田博, 定清直
    2012, 日本分子生物学会年会プログラム・要旨集(Web), 35th, 1LBA-0769 (WEB ONLY), Japanese

  • Ikuo Shoji, Lin Deng, Hak Hotta
    2012, FRONTIERS IN MICROBIOLOGY, 3, English
    [Refereed]
    Book review

  • C型肝炎ウイルス感染によるインスリン抵抗性誘導の分子機序について
    井出良浩, 兼田崇作, 犬伏祥子, 足達哲也, LIN Deng, 勝二郁夫, 堀田博
    2009, 日本ウイルス学会学術集会プログラム・抄録集, 57th

  • C型肝炎ウイルスコア蛋白質の安定性調節因子E6AP及びPA28γの相互作用解析
    山下亮輔, 福田浩一郎, 犬伏祥子, 村上恭子, 鈴木哲朗, 森石恆司, 松浦善治, DENG Lin, 井出良浩, 堀田博, 勝二郁夫
    2009, 日本分子生物学会年会講演要旨集, 32nd(Vol.1) (Vol.1)

  • Sequence variation of Hepatitis C virus subtype 1B and development of hepatocellular carcinoma
    H Hotta, S Ogata, R Hidajat, R Florese, L Deng, M Nagano-Fujii
    Dec. 2003, JOURNAL OF CLINICAL VIROLOGY, 28, S52 - S52, English
    Summary international conference

■ Lectures, oral presentations, etc.
  • HCV-induced ROS/JNK signaling pathway activates the E3 ubiquitin ligase Itch to promote the release of HCV particles via polyubiquitylation of VPS4A.
    Lin Deng, Yujiao Liang, Adi Ariffianto, Chieko Matsui, Takayuki Abe, Masamichi Muramatsu, Takaji Wakita, Hideki Shibata, Masatoshi Maki, Ikuo Shoji
    第68回日本ウイルス学会学術集会, Nov. 2021, Japanese
    Oral presentation

  • Activation of Nrf2/ARE signaling pathway upon hepatitis B virus infection exerts an inhibitory effect on viral replication
    Adi Ariffianto, Lin Deng, Yujiao Liang, Chieko Matsui, Takayuki Abe, Yoshiharu Matsuura, Ikuo Shoji
    2021 International HBV Meeting, Sep. 2021, English
    Poster presentation

  • HCV-induced ROS/JNK signaling pathway activates the E3 ubiquitin ligase Itch to promote the release of HCV particles via polyubiquitylation of VPS4A
    Lin Deng, Yujiao Liang, Adi Ariffianto, Chieko Matsui, Takayuki Abe, Masamichi Muramatsu, Takaji Wakita, Hideki Shibata, Masatoshi Maki, Ikuo Shoji
    the 27th International Symposium on Hepatitis C Virus and Related Viruses, Jul. 2021, English
    Poster presentation

  • Hepatitis B virus X protein activates Nrf2/ARE signaling pathway to suppress viral replication
    Lin Deng, Adi Ariffianto, Yujiao Liang, Chieko Matsui, Takayuki Abe, Yoshiharu Matsuura, Ikuo Shoji
    17th ISVHLD GHS (Global Hepatitis Summit) 2021, Jun. 2021, English
    Oral presentation

  • ISGylation of HBx protein confers the pro-viral effects on HBV replication and resistance to interferon (IFN)-response
    Rheza Gandi Bawono, Takayuki Abe, Qu Mengting, Daisuke Kuroki, Lin Deng, Chieko Matsui, Kunitada Shimotohno, Ikuo Shoji
    第43回日本分子生物学会年会, Dec. 2020
    Poster presentation

  • Screening for anti-hepatitis B virus activity among heterocyclic compounds using HBV-NanoLuc reporter gene
    Daisuke Kuroki, Takayuki Abe, Chieko Matsui, Lin Deng, Norihiko Takeda, Motohiro Yasui, Masafumi Ueda, Takashi Okitsu, Yumiko Yamano, Manabu Hatano, Ikuo Shoji
    第43回日本分子生物学会年会, Dec. 2020
    Poster presentation

  • Annexin 5 participates in the negative regulation of HCV propagation
    Takayuki Abe, Chieko Matsui, Lin Deng, Yoshiharu Matsuura, Ikuo Shoji
    第43回日本分子生物学会年会, Dec. 2020
    Poster presentation

  • Hepatitis B virus X protein induces antioxidant response via activation of Nrf2/ARE signaling pathway
    Adi Ariffianto, Lin Deng, Chieko Matsui, Takayuki Abe, Yoshiharu Matsuura, Ikuo Shoji
    The 43rd Annual Meeting of the Molecular Biology Society of Japan, Dec. 2020
    Poster presentation

  • HCV-induced ROS/JNK signaling pathway activates the E3 ubiquitin ligase Itch to promote the release of HCV particles via polyubiquitylation of VPS4A.
    Lin Deng, Adi Ariffianto, Chieko Matsui, Takayuki Abe, Masamichi Muramatsu, Takaji Wakita, Hideki Shibata, Masatoshi Maki4, Ikuo Shoji
    The 43rd Annual Meeting of the Molecular Biology Society of Japan, Dec. 2020, Japanese, The Molecular Biology Society of Japan, Japan, Domestic conference
    Poster presentation

  • The role of ISG15-conjugation on the Hepatitis B virus HBx protein
    Takayuki Abe, Rheza Gandi Bawono, Lin Deng, Chieko Matsui, Kunitada Shimotohno, Ikuo Shoji
    2018 International HBV Meeting, Oct. 2018, English, Hepatitis B Foundation, シシリー, International conference
    Poster presentation

  • Hepatitis C virus induces the lysosomal degradation of the HNF-1β transcription factor via chaperone-mediated autophagy
    Chieko Matsui, Lin Deng, Takayuki Abe, Ikuo Shoji
    第66回日本ウイルス学会学術集会, Oct. 2018, English, 日本ウイルス学会, 京都, Domestic conference
    Oral presentation

  • HCV-induced activation of JNK/Itch signaling pathway is involved in the release of infectious viral particles.
    Lin Deng, Chieko Matsui, Takayuki Abe, Ikuo Shoji
    The 25th International Symposium on Hepatitis C Virus and Related Viruses, Oct. 2018, English, Organising Committee of the 25th International Symposium on Hepatitis C Virus and Related Viruses, ダブリン, International conference
    Oral presentation

  • HCV-induced activation of JNK/Itch signaling pathway is involved in the release of infectious viral particles.
    Lin Deng, Chieko Matsui, Takayuki Abe, Ikuo Shoji
    第66回日本ウイルス学会学術集会, Oct. 2018, English, 日本ウイルス学会, 京都, Domestic conference
    Public symposium

  • Degradation of HCV-induced HNF-1β protein by chaperone-mediated autophagy
    Chieko Matsui, Lin Deng, Takayuki Abe, Ikuo Shoji
    The 25th International Symposium on Hepatitis C Virus and Related Viruses, Oct. 2018, English, Organising Committee of the 25th International Symposium on Hepatitis C Virus and Related Viruses, ダブリン, International conference
    Poster presentation

  • Critical role of NS5A-ISGylation in the efficient HCV RNA replication
    Takayuki Abe, Nanae Minami, Rheza Gandi Bawono, Chieko Matsui, Lin Deng, Takasuke Fukuhara, Yoshiharu Matsuura, Ikuo Shoji
    The 25th International Symposium on Hepatitis C Virus and Related Viruses, Oct. 2018, English, Organising Committee of the 25th International Symposium on Hepatitis C Virus and Related Viruses, ダブリン, International conference
    Poster presentation

  • Critical role of NS5A-ISGylation in the efficient HCV RNA replication
    Takayuki Abe, Nanae Minami, Rheza Gandi Bawono, Chieko Matsui, Lin Deng, Takasuke Fukuhara, Yoshiharu Matsuura, Ikuo Shoji
    第66回日本ウイルス学会学術集会, Oct. 2018, English, 日本ウイルス学会, 京都, Domestic conference
    Oral presentation

  • C型肝炎ウイルスによる脂肪滴形成機構の解析
    MATSUI CHIEKO, DENG Lin, ABE TAKAYUKI, SHOJI IKUO
    第38回近畿腸管微生物研究会, Jun. 2018, Japanese, 近畿腸管微生物研究会, 大阪, Domestic conference
    Oral presentation

  • Characterization of deubiquitinating enzyme USP15 inhibitor candidates
    Shoji Ikuo, Matsui Chieko, Deng Lin, Abe Takayuki
    Consortium of Biological Sciences 2017, Dec. 2017, English, The Molecular Biology Society of Japan, 神戸, Domestic conference
    Poster presentation

  • Novel equine-like G3 rotavirus strains among children in Surabaya, Indonesia, 2015-2016
    Rury Mega Wahyuni, Utsumi Takako, Yen Hai Doan, Zayyin Dinana, 藤井 克樹, Soegeng Soegijanto, Juniastuti, Laura Navika Yamani, Matsui Chieko, Deng Lin, Abe Takayuki, Soetjipto, Maria Inge Lusida, 片山 和彦, Shoji Ikuo
    The 65th Annual Meeting of the Japanese Society for Virology, Oct. 2017, English, Japanese Society for Virology, 大阪, Domestic conference
    Poster presentation

  • Norovirus infection in an asymptomatic population in Indonesia
    Utsumi Takako, Maria Inge Lusida, Zayyin Dinana, Rury Mega Wahyuni, Laura Navika, Yamani, Juniastuti, Soetjipto, Matsui Chieko, Deng Lin, Abe Takayuki, Yen Hai Doan, 藤井 克樹, 片山 和彦, Shoji Ikuo
    The 65th Annual Meeting of the Japanese Society for Virology, Oct. 2017, English, Japanese Society for Virology, 大阪, Domestic conference
    Poster presentation

  • Interferon-stimulated gene 15 (ISG15) regulates HCV RNA replication via different ISGylation sites on HCV NS5A
    Abe Takayuki, 南 奈苗, 友近 拳, Matsui Chieko, Deng Lin, 福原 崇介, 松浦 善治, Shoji Ikuo
    The 65th Annual Meeting of the Japanese Society for Virology, Oct. 2017, English, The Japanese Society for Virology, 大阪, Domestic conference
    Public symposium

  • Hepatitis C virus NS3/4A protease cleaves SGP20 and promotes lipid droplet growth
    Matsui Chieko, 南 奈苗, Deng Lin, Abe Takayuki, Shoji Ikuo
    The 65th Annual Meeting of the Japanese Society for Virology, Oct. 2017, Japanese, Japanese Society for Virology, 大阪, Domestic conference
    Poster presentation

  • HCV infection promotes Itch ubiquitin ligase activity via activation of JNK and modulates release of infectious viral particles.
    Deng Lin, Matsui Chieko, Abe Takayuki, Shoji Ikuo
    The 65th Annual Meeting of the Japanese Society for Virology, Oct. 2017, English, The Japanese Society for Virology, 大阪, Domestic conference
    Public symposium

  • Peroxiredoxin 1, a novel HBx-interacting protein, negatively regulates HBV replication through binding to HBV RNA for HBV RNA degradation
    Deng Lin, Ming Chen, Matsui Chieko, Abe Takayuki, Hak Hotta, Shoji Ikuo
    2017 International HBV Meeting., Sep. 2017, English, Organising Committee of 2017 International Meeting on Molecular Biology of Hepatitis B Viruses, Washington DC, USA, International conference
    Oral presentation

  • Interferon-stimulated gene 15 (ISG15) regulates HCV RNA replication via different ISGylation sites on HCV NS5A
    Abe Takayuki, 南 奈苗, 友近 拳, Matsui Chieko, Deng Lin, 福原 崇介, 松浦 善治, Shoji Ikuo
    The 24th International Symposium on Hepatitis C virus and Related Viruses, Sep. 2017, English, Organising Committee of the 24th International Symposium on Hepatitis C Virus and Related Viruses, Massachusetts, USA, International conference
    Poster presentation

  • HCV infection promotes Itch ubiquitin ligase activity via activation of JNK and modulates release of infectious viral particles.
    Deng Lin, Matsui Chieko, Abe Takayuki, Shoji Ikuo
    The 24th International Symposium on Hepatitis C Virus and Related Viruses, Sep. 2017, English, Organising Committee of the 24th International Symposium on Hepatitis C Virus and Related Viruses, Washington DC, USA, International conference
    Poster presentation

  • A novel pathway for lipid droplet formation induced by hepatitis C virus
    Matsui Chieko, Nanae Minami, Deng Lin, Abe Takayuki, Shoji Ikuo
    24th International Symposium on Hepatitis C Virus and Related Viruses, Sep. 2017, English, Organising Committee of the 24th International Symposium on Hepatitis C Virus and Related Viruses, Cape Cod, USA, International conference
    Poster presentation

  • Norovirus and Rotavirus Infections among Hospitalized Children with Acute Gastroenteritis in Surabaya, East Java, Indonesia
    Laura Navika Yamani, Utsumi Takako, Soegeng Soegijanto, Zayyin Dinana, Rury Mega, Wahyuni, Juniastuti, Matsui Chieko, Deng Lin, Abe Takayuki, Yen Hai Doan, Soetjipto, Kazuhiko Katayama, Maria Inge Lusida, Shoji Ikuo
    2nd Molecular, Cellular, and Life Sciences 2017, Jul. 2017, English, Osaka University and Universitas Airlangga, Surabaya, Indonesia, International conference
    Oral presentation

  • Selective protein degradation via HCV-induced chaperone mediated autophagy
    Shoji Ikuo, Matsui Chieko, Deng Lin, Abe Takayuki
    第37回近畿腸管微生物研究会, Jun. 2017, Japanese, 近畿腸管微生物研究会, 大阪, Domestic conference
    Oral presentation

  • Screening for deubiquitinating enzyme USP15 inhibitors and their characterization
    Shoji Ikuo, Deng Lin, Chieko Matsui, Nanae Minami, Takayuki Abe
    The 39th Annual Meeting of the Molecular Biology Society of Japan, Nov. 2016, English, The Molecular Biology Society of Japan, 横浜, Domestic conference
    Poster presentation

  • Upregulation of MAPK phosphatase 3 is involved in HCV-induced dephosphorylation of FoxO1.
    Deng Lin, Ming Chen, Shoji Ikuo, Hak Hotta
    The 23rd International Symposium on Hepatitis C Virus and Related Viruses, Oct. 2016, English, Organising Committee of the 23rd International Symposium on Hepatitis C Virus and Related Viruses, Kyoto, Japan, International conference
    Poster presentation

  • Upregulation of MAPK phosphatase 3 is involved in HCV-induced dephosphorylation of FoxO1.
    Deng L, Chen M, Shoji I, HOTTA HAK
    23rd International Symposium on Hepatitis C Virus and Related Viruses, Oct. 2016, English, Kyoto, International conference
    Poster presentation

  • Two different roles of ISG15 in HCV infection
    Nanae Minami, Tutik Wahyuni Sri, Chieko Matsui, Deng Lin, Shoji Ikuo
    The 64th Annual Meeting of the Japanese Society for Virology, Oct. 2016, English, The Japanese Society for Virology, 札幌, Domestic conference
    Poster presentation

  • Peroxiredoxin 1, a novel HBx-interacting protein, negatively regulates HBV replication through acceleration of HBV RNA degradation.
    DENG Lin, GAN Xiang, CHEN Ming, SHOJI Ikuo, HOTTA Hak
    The 64th Annual Meeting of the Japanese Society for Virology, Oct. 2016, English, The Japanese Society for Virology, 札幌, Domestic conference
    Public symposium

  • Molecular mechanism of HCV-induced lysosomal degradation of HNF-1α protein
    Chieko Matsui, Nanae Minami, Deng Lin, Shoji Ikuo
    The 23rd International symposium on Hepatitis C Virus and Related Viruses, Oct. 2016, English, Organising Committee of the 23rd International Symposium on Hepatitis C Virus and Related Viruses, Kyoto, Japan, International conference
    Poster presentation

  • C型肝炎ウイルスによるHNF-1α蛋白質の選択的分解機構
    松井 千絵子, 南 奈苗, Deng Lin, Shoji Ikuo
    The 64th Annual Meeting of the Japanese Society for Virology, Oct. 2016, English, The Japanese Society for Virology, 札幌, Domestic conference
    Oral presentation

  • Antiviral activities of the scorpine-like peptide Smp 76 isolated from Scorpio maurus palmatus against dengue virus and hapatitis C virus.
    HOTTA HAK, El-Bitar AA, Sarhan MM, Rahman MA, Possani LD, Chen M, Deng L, Utsubo CA
    23rd International Symposium on Hepatitis C Virus and Related Viruses, Oct. 2016, English, Kyoto, International conference
    Poster presentation

  • Anti-hepatitis C virus compounds from Ruta angustifolia mediate a synergistic effect in combination with current direct-acting antiviral agents.
    Wahyuni T S, Widyawaruyanti A, Lusida MI, Fuad A, Deng L, Matsui C, Fuchino H, Kawahara N, Shoji I, HOTTA HAK
    23rd International Symposium on Hepatitis C Virus and Related Viruses, Oct. 2016, English, Kyoto, International conference
    Poster presentation

  • Peroxiredoxin 1 is a guardian of the host cell against HBV infection.
    Deng Lin, Xiang Gan, Ming Chen, Ikuo Shoj, Hak Hotta
    2016 International HBV Meeting., Sep. 2016, English, Organising Committee of 2016 International Meeting on Molecular Biology of Hepatitis B Viruses, Seoul, Korea, International conference
    Poster presentation

  • Peroxiredoxin 1 is a guardian of the host cell against HBV infection.
    Deng L, GAN XIANG, Chen M, Shoji I, HOTTA HAK
    2016 International HBV Meeting. The Molecular Biology of Hepatitis B Viruses, Sep. 2016, English, Seoul, International conference
    Poster presentation

  • Occurrence of norovirus infection in an asymptomatic population in Indonesia
    Zayyin Sinana, Utsumi Takako, Rury Mega Wahuni, Laura Navika Yamani, Chieko Matsui, Deng Lin, Maria Inge Lusida, Soetjipto, Yen, Hai Doan, Kazuhiko Katayama, Shoji Ikuo
    Intenational seminar Global Strategy to Combat Emerging Infectious Diseases in Borderless Era, Aug. 2016, English, Faculty of Medicine and Institute of Tropical Disease, Universitas Airlangga, スラバヤ, インドネシア, International conference
    Oral presentation

  • A preliminary survey of norovirus and rotavirus infections among children in Surabaya, Indonesia
    Soetjipto, Utsumi Takako, Maria Inge Lusida, Rury Mega Wahuni, Zayyin Dinana, Juniastuti, Laura Navika Yamani, Subijanto Marto Sudarmo, Alpha Fardah Athiyyah, Andi Darma, Chieko Matsui, Deng Lin, Yen Hai Doan, Kazuhiko Katayama, Shoji Ikuo
    Intenational seminar Global Strategy to Combat Emerging Infectious Diseases in Borderless Era, Aug. 2016, English, Faculty of Medicine and Institute of Tropical Disease, Universitas Airlangga, スラバヤ, インドネシア, International conference
    [Invited]
    Invited oral presentation

  • Up-regulation of MAPK phosphatase 3 is involved in HCV-induced dephosphorylation of FoxO1.
    Deng Lin, GAN XIANG, Chen M, Shoji Ikuo, Hotta Hak
    The 11th Japan-China International Conference of Virology, Jul. 2016, English, 日中国際ウイルス学会世話人, 観音時, International conference
    Oral presentation

  • Up-regulation of MAPK phosphatase 3 is involved in HCV-induced dephosphorylaion of FoxO1.
    Deng Lin, Ming Chen, Shoji Ikuo, Hak Hotta
    The 11th Japan-China International Conference of Virology, Jul. 2016, English, Organising Committee of The 11th Japan-China International Conference of Virology, Kanonji, Japan, International conference
    Oral presentation

  • Peroxiredoxin 1 negatively regulates hepatitis B virus replication through interaction with HBx.
    Deng Lin, Xiang Gan, Ming Chen, Ikuo Shoj, Hak Hotta
    The 4th JAPAN-TAIWAN Research Symposium on Hepatitis B Virus, Apr. 2016, English, Organising Committee of The 4th JAPAN-TAIWAN Research Symposium on Hepatitis B Virus, Taipei, Taiwan, International conference
    Public symposium

  • Peroxiredoxin 1 negatively regulates hepatitis B virus replication through interaction with HBx.
    Deng Lin, GAN XIANG, Chen M, Shoji Ikuo, Hotta Hak
    4th JAPAN-TAIWAN Research Symposium on Hepatitis B Virus, Apr. 2016, English, Taiwan Association for the study of the Liver, Taipei, Taiwan, International conference
    [Invited]
    Invited oral presentation

  • Screening for small molecule inhibitors of deubiquitinating enzyme USP15
    Shoji Ikuo, Sianipar Imelda Rosalyn, 南 奈苗, 陳 明, 松井 千絵子, Deng Lin
    BMB2015 Biochemistry and Molecular Biology, Dec. 2015, Japanese, 日本分子生物学会、日本生化学会, 神戸, Domestic conference
    Poster presentation

  • Peroxiredoxin 1, a novel binding partner of HBx, is a negative regulator of HBV replication
    Deng Lin, Xiang Gan, Ikuo Shoj, Hak Hotta
    The 63rd Annual Meeting of the Japanese Society for Virology, Nov. 2015, English, The Japanese Society for Virology, 福岡, Domestic conference
    Oral presentation

  • A novel pathway for lipid droplet formation induced by hepatitis C virus
    松井 千絵子, Imelda Rosalyn Sianipar, 南 奈苗, 陳 明, Deng Lin, 堀田 博, Shoji Ikuo
    The 63rd Annual Meeting of the Japanese Society for Virology, Nov. 2015, English, The Japanese Society for Virology, 福岡, Domestic conference
    Oral presentation

  • Physical and functional interaction between hepatitis C virus NS5A protein and ovarian tumor protein deubiquitinase 7B
    Imelda R Sianipar, Chieko Matsui, Nanae Minami, Ming Chen, Xiang Gan, Deng Lin, Hak Hotta, Shoji Ikuo
    22th International Symposium on Hepatitis C Virus and Related Viruses, Oct. 2015, English, Organising Committee of the22th International Symposium on Hepatitis C Virus and Related Viruses, Strasbourg, France, International conference
    Poster presentation

  • Peroxiredoxin 1 negatively regulates hepatitis B virus replication through interaction with HBx
    Deng Lin, Xiang Gan, Ikuo Shoj, Hak Hotta
    2015 International Meeting on Molecular Biology of Hepatitis B Viruses, Oct. 2015, English, Organising Committee of 2015 International Meeting on Molecular Biology of Hepatitis B Viruses, Bad Nauheim, Germany, International conference
    Poster presentation

  • MAPK phosphatase 3 is involved in HCV-induced dephosphorylaion of FoxO1
    Deng Lin, Ming Chen, Shoji Ikuo, Hak Hotta
    22th International Symposium on Hepatitis C Virus and Related Viruses, Oct. 2015, English, Organising Committee of the22th International Symposium on Hepatitis C Virus and Related Viruses, Strasbourg, France, International conference
    Poster presentation

  • A single-amino-acid mutation in hepatitis C virus NS5A disrupts physical and functional interaction with the transcription factor HNF-1α
    松井 千絵子, Imelda Rosalyn Sianipar, 南 奈苗, Deng Lin, 堀田 博, Shoji Ikuo
    22nd International symposium on Hepatitis C Virus and Related Viruses, Oct. 2015, English, HCV2015 Organising committee, Strasbourg, France, International conference
    Poster presentation

  • Ｃ型肝炎ウイルスによるミトコンドリア介在性アポトーシス誘導機構の解明.
    甘 翔, Deng Lin, 陳 明, Shoji Ikuo, Hotta Hak
    第62回日本ウイルス学会学術集会., Nov. 2014, Japanese, 日本ウイルス学会, 横浜, Domestic conference
    Oral presentation

  • HCV NS5A protein physically and functionally interacts with an OTU deubiquitinase.
    Sianipar I R, Shoji Ikuo, Matsui C, Minami N, Deng Lin, Hotta Hak
    第62回日本ウイルス学会学術集会., Nov. 2014, English, 日本ウイルス学会, 横浜, Domestic conference
    Poster presentation

  • HCV NS5A interacts with lysine methyltransferase SMYD3 and transcriptionally activates the protein disulfide isomerase gene AGR3.
    Ming Chen, Xiang Gan, Deng Lin, Shoji Ikuo, Hotta Hak
    第62回日本ウイルス学会学術集会., Nov. 2014, English, 日本ウイルス学会, 横浜, Domestic conference
    Oral presentation

  • C型肝炎ウイルス感染によるTGF-βスーパーファミリーにおけるSmad2/3とSmad1/5/9経路の脱制御とその分子機序の解明.
    松岡陽子, Deng Lin, 朝日朱美, Aoki Chie, Shoji Ikuo, Hotta Hak
    第62回日本ウイルス学会学術集会., Nov. 2014, Japanese, 日本ウイルス学会, 横浜, Domestic conference
    Oral presentation

  • C型肝炎ウイルス感染によるHepatocyte nuclear factor (HNF) -1α蛋白質の選択的分解機構.
    松井千絵子, Shoji Ikuo, Sianipar I R, 南 奈苗, Deng Lin, Hotta Hak
    第62回日本ウイルス学会学術集会., Nov. 2014, Japanese, 日本ウイルス学会, 横浜, Domestic conference
    Poster presentation

  • C型肝炎ウイルスによるHNF-1α蛋白質の選択的分解機構の解析
    Shoji Ikuo, 松井千絵子, Imelda Rosalyn Sianipar, 南奈苗, Deng Lin, Hotta Hak
    第37回日本分子生物学会年会, Nov. 2014, Japanese, 日本分子生物学会, 横浜, Domestic conference
    Poster presentation

  • B型肝炎ウイルスXタンパク質の新規結合因子抗酸化酵素ペルオキシレドキシン1(Prdx1)の同定と機能解析.
    Deng Lin, 甘 翔, 篠崎健太, Shoji Ikuo, Hotta Hak
    第62回日本ウイルス学会学術集会., Nov. 2014, Japanese, 日本ウイルス学会, 横浜, Domestic conference
    Oral presentation

  • B型肝炎ウイルスXタンパク質とヒストンメチル基転移酵素SMYD3の相互作用の解析.
    林美和子, Deng Lin, 篠崎健太, 陳 明, Shoji Ikuo, Hotta Hak
    第62回日本ウイルス学会学術集会., Nov. 2014, Japanese, 日本ウイルス学会, 横浜, Domestic conference
    Poster presentation

  • Physical and functional interaction between an OTU deubiquitinase and HCV NS5A protein.
    Sianipar Imelda Rosalyn, Shoji Ikuo, Matsui Chieko, Minami Nanamia, Deng Lin, Hotta Hak
    21th International Symposium on Hepatitis C Virus and Related Viruses., Sep. 2014, English, Organising Committee of the 21th International Symposium on Hepatitis C Virus and Related Viruses, Banff, Banff, International conference
    Poster presentation

  • Peroxiredoxin 1 is a novel binding partner of HBx and a positive regulator of hepatitis B virus transcription.
    Deng Lin, Xiang Gan, Kenta Shinozaki, Shoji Ikuo, Hotta Hak
    2014 International Meeting on Molecular Biology of Hepatitis B Viruses., Sep. 2014, English, Organising Committee of the 2014 International Meeting on Molecular Biology of Hepatitis B Viruses., Los Angeles, International conference
    Oral presentation

  • NS5B induces up-regulation of the BH3-only protein, BIK, essential for the Hepatitis C virus RNA replication and viral release.
    Ching Wooen Sze, Jude Juventus Aweya, Anthony Bayega, Nur Khairiah Mohd-Ismail, Deng Lin, Hotta Hak, Yee-Joo Tan
    21th International Symposium on Hepatitis C Virus and Related Viruses., Sep. 2014, English, Organising Committee of the 21th International Symposium on Hepatitis C Virus and Related Viruses, Banff, Banff, International conference
    Poster presentation

  • Interaction between HBx and lysine methyltransferase SMYD3, a novel HBx-interacting protein.
    Deng Lin, Miwako Hayashi, Kenta Shinozaki, Ming Chen, Shoji Ikuo, Hotta Hak
    2014 International Meeting on Molecular Biology of Hepatitis B Viruses., Sep. 2014, English, Organising Committee of the 2014 International Meeting on Molecular Biology of Hepatitis B Viruses., Los Angeles, International conference
    Poster presentation

  • HCV induces Bim/Bax-mediated apoptosis through the ROS/JNK signaling pathway.
    Deng Lin, Ming Chen, Shoji Ikuo, Hotta Hak
    21th International Symposium on Hepatitis C Virus and Related Viruses., Sep. 2014, English, Organising Committee of the 21th International Symposium on Hepatitis C Virus and Related Viruses, Banff, Canada, International conference
    Poster presentation

  • HCV dysregulates Smad2/3- and Smad1/5-signaling pathways of the TGF-β superfamily.
    Yoko Matsuoka, Deng Lin, Akemi Asahi, Aoki Chie, Shoji Ikuo, Hotta Hak
    21th International Symposium on Hepatitis C Virus and Related Viruses., Sep. 2014, English, Organising Committee of the 21th International Symposium on Hepatitis C Virus and Related Viruses, Banff, Banff, International conference
    Poster presentation

  • Determinants of specific interaction between hepatitis C virus NS5A and HNF-1α protein.
    Matsui Chieko, Shoji Ikuo, Sianipar Imelda Rosalyn, Minami Nanami, Deng Lin, Hotta Hak
    21th International Symposium on Hepatitis C Virus and Related Viruses., Sep. 2014, English, Organising Committee of the 21th International Symposium on Hepatitis C Virus and Related Viruses, Banff, Banff, International conference
    Poster presentation

  • A tandem affinity purification analysis of HBx-interacting proteins and identification of two novel interactors Prdx1 and SMYD3.
    Deng Lin, Xiang Gan, Miwako Hayashi, Kenta Shinozaki, Ming Chen, Shoji Ikuo, Hotta Hak
    2014 TASL-Japan Hepatitis B workshop., Apr. 2014, English, Taiwan Association for the study of the Liver, Taipei, Taiwan, International conference
    [Invited]
    Invited oral presentation

  • Ｃ型肝炎ウイルス感染によるBax活性化の分子機序の解析
    Deng Lin, 陳 明, Shoji Ikuo, Hotta Hak
    第61回日本ウイルス学会学術集会, Nov. 2013, Japanese, 日本ウイルス学会, 神戸, Domestic conference
    Oral presentation

  • HCV感染による糖代謝障害の分子機序
    Shoji Ikuo, 松井 千絵子, Deng Lin, Hotta Hak
    第61回日本ウイルス学会学術集会, Nov. 2013, Japanese, 日本ウイルス学会, 神戸, Domestic conference
    [Invited]
    Nominated symposium

  • HCV NS5AとHepatocyte nuclear factor (HNF) -1αの相互作用と病態生理
    松井 千絵子, Shoji Ikuo, 南 奈苗, Sianipar Imelda Rosalyn, Deng Lin, Hotta Hak
    第61回日本ウイルス学会学術集会, Nov. 2013, Japanese, 日本ウイルス学会, 神戸, Domestic conference
    Poster presentation

  • C型肝炎ウイルス非構造蛋白質NS5AにおけるFyn-SH2ドメインとの結合に重要なチロシン残基同定の試み
    竹内 健司, 孫 雪東, 千原 一泰, Deng Lin, Shoji Ikuo, Hotta Hak, 定 清直
    第61回日本ウイルス学会学術集会, Nov. 2013, Japanese, 日本ウイルス学会, 神戸, Domestic conference
    Poster presentation

  • C型肝炎ウイルス感染によるSmad1/Smad5経路の脱制御とその分子機序について
    松岡 陽子, 朝日 朱美, Deng Lin, Shoji Ikuo, Hotta Hak
    第61回日本ウイルス学会学術集会, Nov. 2013, Japanese, 日本ウイルス学会, 神戸, Domestic conference
    Poster presentation

  • Chlorophill分解産物Pheophorbide a、Chlorin e6及び半合成誘導体Mono-L-aspartyl chlorin e6 (NPe6) はC型肝炎ウイルス増殖を阻害する
    Suratno Lulut Ratnoglik, Aoki Chie, 河本 真理, Pratiwi Sudarmono, Deng Lin, Shoji Ikuo, 渕野 裕之, 川原 信夫, Hotta Hak
    第61回日本ウイルス学会学術集会, Nov. 2013, Japanese, 日本ウイルス学会, 神戸, Domestic conference
    Poster presentation

  • Regulation of hepatocyte nuclear factor 1α by hepatitis C virus NS5A protein
    Chieko Matsui, Shoji Ikuo, Nanae Minami, Imelda Rosalyn Sianipar, Deng Lin, Hotta Hak
    20th International Symposium on Hepatitis C Virus and Related Viruses., Oct. 2013, English, Organising Committee of the20th International Symposium on Hepatitis C Virus and Related Viruses, Melbourne, Australia, International conference
    Poster presentation

  • HCV upregulates Bim through ROS/JNK signaling pathway leading to Bax-mediated apoptosis
    Deng Lin, Ming Chen, Shoji Ikuo, Hotta Hak
    20th International Symposium on Hepatitis C Virus and Related Viruses., Oct. 2013, English, Organising Committee of the20th International Symposium on Hepatitis C Virus and Related Viruses, Melbourne, Australia, International conference
    Oral presentation

  • HCV NS5A interacts with SMYD3 and upregulates SMYD3-mediated expression of AGR3 mRNA
    Ming Chen, Xiang Gan, Deng Lin, Shoji Ikuo, Hotta Hak
    20th International Symposium on Hepatitis C Virus and Related Viruses., Oct. 2013, English, Organising Committee of the20th International Symposium on Hepatitis C Virus and Related Viruses, Melbourne, Australia, International conference
    Poster presentation

  • Development of a prophylactic and therapeutic vaccine against Hepatitis C virus
    Suratno Lulut Ratnoglik, Jiang Dapeng, Aoki Chie, Pratiwi Sudarmono, Deng Lin, Shoji Ikuo, Hotta Hak
    20th International Symposium on Hepatitis C Virus and Related Viruses., Oct. 2013, English, Organising Committee of the20th International Symposium on Hepatitis C Virus and Related Viruses, Melbourne, Australia, International conference
    Poster presentation

  • Antiviral activity of chlorophyll derivatives, pheophorbide a, chlorin e6 and mono-L-aspartyl chlorin e6 (NPe6), against hepatitis C virus
    Hotta Hak, Aoki Chie, Suratno Lulut Ratnoglik, Pratiwi Sudarmono, Mari Komoto, Deng Lin, Shoji Ikuo, Hiroyuki Fuchino, Nobuo Kawahara
    20th International Symposium on Hepatitis C Virus and Related Viruses., Oct. 2013, English, Organising Committee of the20th International Symposium on Hepatitis C Virus and Related Viruses, Melbourne, Australia, International conference
    Poster presentation

  • Hepatitis C virus infection suppresses GLUT2 gene expression via down-regulation of hepatocyte nuclear factor 1α
    Shoji Ikuo, 松井千絵子, 兼田祟作, Imelda Rosalyn Sianipar, Deng Lin, Hotta Hak
    The 35th Annual Meeting of the Molecular Biology Society of Japan, Dec. 2012, Japanese, The Molecular Biology Society of Japan, 福岡, Hepatitis C virus (HCV) infection causes not only intrahepatic diseases but also extrahepatic manifestations, including type 2 diabetes. We previously reported that HCV replication suppresses cellular glucose uptake by down-regulation of cell surface expr, Domestic conference
    Oral presentation

  • C 型肝炎ウイルスNS5A 蛋白質のSrc homology 2/3 ドメイン結合能とB 細胞での発現によるSrc ファミリーキナーゼFyn の活性化
    中島 謙治, 竹内 健司, 千原 一泰, 堀口 朋子, 孫 雪東, Deng Lin, Shoji Ikuo, Hotta Hak, 定 清直
    第35回日本分子生物学会年会, Dec. 2012, Japanese, 日本分子生物学会, 福岡, C 型肝炎ウイルス（HCV）は肝細胞以外にB 細胞にも感染し、慢性肝炎の合併症として混合型クリオグロブリン血症や非ホジキンリンパ腫を引き起こすが、発症機序は不明である。今回、我々は、HCV 非構造蛋白質NS5A のB 細胞に対する影響を検討するため、エピトープタグを付加したNS5A を安定発現するB 細胞株を樹立した。この細胞を蛋白質チロシンフォスファターゼ阻害剤であるPervanadate で処理したところ、NS5A がチロシンリン酸化されることを見出した。チロシンリン酸化蛋白質と結合する蛋白質ドメインとしてSrc homology 2 (SH2) が知られており、B 細胞受容体を介するシグナル伝達経路中にもこのドメインを持つ蛋白質がいくつかある。そこで、これらのNS5A 結合能をプルダウンアッセイ法で検討し、Src ファミリーキナーゼFyn 由来, Domestic conference
    Poster presentation

  • Ｃ型肝炎ウイルス感染による転写因子FoxO1脱リン酸化の分子機序の解析
    Deng Lin, 金子 昌裕, 河本 真理, Jiang Dapeng, Shoji Ikuo, Hotta Hak
    第60回日本ウイルス学会学術集会, Nov. 2012, Japanese, 日本ウイルス学会, 大阪, 【目的と意義】C型肝炎ウイルス（HCV）の慢性感染は2型糖尿病の発症に関与することが知られているが、その分子機序は不明な点が多い。我々は昨年本会において、1) HCV感染が酸化ストレス誘導を介してJNKを活性化し、糖新生制御因子である転写因子FoxO1のリン酸化を抑制し、活性化状態を持続させること、2) 活性化されたFoxO1により、糖新生律速酵素遺伝子群の転写が促進され、肝細胞の糖新生が亢進することを報告した。HCVによるFoxO1の脱制御（強制持続的活性化）において、通常の糖新生制御経路インスリンレセプター–PI3キナーゼ–Akt/PKBシグナル経路の制御を受けないことから、それ以外のFoxO1リン酸化・脱リン酸化経路の関与が強く示唆された。近年、FoxO1の脱リン酸化の分子機序として、MAPK phosphatase-3 (MKP3)及びpro, Domestic conference
    Oral presentation

  • Ｃ型肝炎ウイルス感染によるBax活性化の分子機序の解析
    Deng Lin, Shoji Ikuo, Hotta Hak
    第65回日本細菌学会関西支部総会, Nov. 2012, Japanese, 日本細菌学会関西支部, 神戸, 【目的】Ｃ型肝炎ウイルス (HCV)は肝臓に慢性の炎症を起こし、高率に肝細胞癌を引き起こすが、その一方で、Ｃ型慢性肝炎患者において肝細胞のアポトーシスの亢進が認められている。我々は、Huh7.5細胞を用いたHCV J6/JFH1感染系で、HCV感染がBaxの活性化を引き起こし、ミトコンドリア障害を介したアポトーシスを誘導すること、及びreactive oxygen species (ROS)の産生を介してc-Jun N-terminal kinase (JNK)経路を活性化することを報告した。一方、アポトーシス促進因子であるBim は、Baxの活性化を促進することが知られている。そこで本研究では、HCV感染によるBax活性化の分子機構を明らかにすることを目的として、ROS/JNK経路及びBimの関与について検討を行った。【方法】HCV J6/JFH1, Domestic conference
    Oral presentation

  • Molecular mechanism of hepatitis C virus-induced glucose metabolism disorder
    Shoji Ikuo, Deng Lin, Matsui Chieko, Hotta Hak
    The 10th JSH Single Topic Conference, Nov. 2012, English, The Japan Society of Hepatology, 東京, Hepatitis C virus (HCV) infection causes not only intrahepatic diseases but also extrahepatic manifestations, including metabolic disorders. Chronic HCV infection is often associated with type 2 diabetes. However, the precise mechanism underlying this ass, Domestic conference
    [Invited]
    Invited oral presentation

  • C型肝炎ウイルスに対する予防および治療ワクチン開発に関する研究
    Jiang Dapeng, Ratnoglik Lulut Suratno, Aoki Chie, Deng Lin, Shoji Ikuo, Hotta Hak
    第60回日本ウイルス学会学術集会, Nov. 2012, Japanese, 日本ウイルス学会, 大阪, 【目的と意義】Ｃ型肝炎ウイルス（HCV）慢性感染者は、日本で約200万人、全世界で約1億7,000万～2億人と推定されている。最近認可されたより治療効果の高い三者併用療法でも、30%近い症例で完全治癒が望めず、HCV 治療ワクチンと新たな感染者発生を防止する予防ワクチンの開発が強く求められている。我々は、HCVに対する予防ワクチンと治療ワクチンを開発する目的で、HCVのエンベロープタンパク質及び非構造タンパク質の一部をコードする遺伝子領域を組み込んだ発現プラスミドを数種類作製し、DNAワクチンとしてマウスに接種して、中和抗体産生及び細胞性免疫誘導を検討した。【材料と方法】1）DNAワクチン：HCV(1b型)のエンベロープタンパク質(E2)及び非構造タンパク質の一部(NS3)をコードする遺伝子領域を組み込んだ発現プラスミドを数種類作製した。2）マウス免, Domestic conference
    Oral presentation

  • C型肝炎ウイルスによるGLUT2遺伝子発現抑制の分子機構
    松井 千絵子, Shoji Ikuo, Deng Lin, Hotta Hak
    第60回日本ウイルス学会学術集会, Nov. 2012, Japanese, 日本ウイルス学会, 大阪, 【目的と意義】C型肝炎ウイルス(HCV)感染が高率にII型糖尿病を合併することが知られているが、詳しい発症機序はいまだ明らかではない。昨年、我々は本会において、HCV感染により細胞内の転写因子Hepatocyte nuclear factor-1α (HNF-1α)の転写が抑制されることが、GLUT2遺伝子転写抑制の原因の一つであることを報告した。その後の検討から、HCV感染によりHNF-1α蛋白質の分解誘導が引き起こされることを見出したので、その分子機序について報告する。【材料と方法】1) HCVによるHNF-1α蛋白質量の減少に蛋白質分解が関与するかを検討するために、各種阻害剤の影響を解析した。ヒト肝がん細胞株Huh-7.5細胞にHCV J6/JFH-1を感染させ、回収12時間前にライソソーム阻害剤またはプロテアソーム阻害剤を投与し、内在性HNF, Domestic conference
    Oral presentation

  • C型肝炎ウイルスNS5A蛋白質の新規結合因子ヒストンメチル基転移酵素SMYD3の同定と機能解析
    陳 明, 甘 翔, Deng Lin, Shoji Ikuo, Hotta Hak
    第60回日本ウイルス学会学術集会, Nov. 2012, Japanese, 日本ウイルス学会, 大阪, 【目的と意義】C型肝炎ウイルス（HCV）は高率に持続感染し、慢性肝炎、肝硬変、肝細胞癌を引き起こす。HCVの非構造蛋白質の一つであるNS5Aはウイルスゲノム複製複合体の主構成因子であるだけでなく、HCVの病原性、ウイルス粒子産生、及びインターフェロン抵抗性に重要な役割を果たしている。しかしながら、その詳細な分子機序は未だ明らかにされていない。本研究では、NS5Aと結合する新規宿主因子を同定し、NS5Aによる新たな病原性発現機構を明らかにすることを目的とした。【材料と方法】 C-末端にMyc-His6タグを付加したNS5AをHuh-7細胞に発現させ、2段階タンデムタグ精製法と質量分析法により、NS5Aと結合する新規宿主因子を探索した。NS5A一過性発現Huh-7.5細胞およびHCV全長レプリコン細胞、HCV J6/JFH1感染細胞を用い、NS5Aと新規, Domestic conference
    Oral presentation

  • Up-regulation of MAPK phosphatase 3 is involved in HCV-induced suppression of FoxO1 phosphorylation.
    Deng Lin, Chen Ming, Jiang Depeng, Shoji Ikuo, Hotta Hak
    19th International Symposium on Hepatitis C Virus and Related Viruses., Oct. 2012, English, Organising Committee of the19th International Symposium on Hepatitis C Virus and Related Viruses, Venice, Italy, Chronic hepatitis C virus (HCV) infection is often associated with type 2 diabetes. We have recently reported that HCV infection promotes hepatic gluconeogenesis through a transcription factor forkhead box O1 (FoxO1)-dependent pathway. We demonstrated that HCV infection induced c-Jun N-terminal kinase (JNK) activation via increased mitochondrial reactive oxygen species (ROS) pr, International conference
    Oral presentation

  • Identification and characterization of a novel NS5A-interacting protein, SMYD3.
    Chen Ming, Gan Xiang, Deng Lin, Shoji Ikuo, Hotta Hak
    19th International Symposium on Hepatitis C Virus and Related Viruses., Oct. 2012, English, Organising Committee of the19th International Symposium on Hepatitis C Virus and Related Viruses, Venice, Italy, Hepatitis C virus (HCV) infection is associated with the development of hepatocellular carcinoma (HCC). Increasing experimental evidence suggests that HCV contributes to HCC by directly modulating pathways that promote the malignant transformation of hepatocytes. HCV non-structural protein 5A (NS5A) is associated with a wide range of cellular proteins involved in cellular signa, International conference
    Poster presentation

  • HCV infection induces lysosomal degradation of hepatocyte nuclear factor 1α via interaction with HCV NS5A protein.
    Matsui Chieko, Shoji Ikuo, Deng Lin, Hotta Hak
    19th International Symposium on Hepatitis C Virus and Related Viruses., Oct. 2012, English, Organising Committee of the19th International Symposium on Hepatitis C Virus and Related Viruses, Venice, Italy, Hepatitis C virus (HCV) infection causes not only intrahepatic diseases but also extrahepatic manifestations, including metabolic disorders and autoimmune diseases. A number of studies have shown that HCV infection often predisposes the host towards type 2 diabetes. We previously reported that HCV replication suppresses cellular glucose uptake through down-regulation of cell su, International conference
    Poster presentation

  • Development of therapeutic and preventive vaccines against Hepatitis C virus.
    Jiang Depeng, Ratnoglik Suratno Lulut, Aoki Chie, Deng Lin, Shoji Ikuo, Hotta Hak
    19th International Symposium on Hepatitis C Virus and Related Viruses., Oct. 2012, English, Organising Committee of the19th International Symposium on Hepatitis C Virus and Related Viruses, Venice, Italy, An estimated 170 to 200 million individuals are chronically infected with Hepatitis C virus (HCV) worldwide and 3 to 4 million individuals are newly infected each year. There is currently no vaccine available to protect against HCV. Considering the limited efficacy and high cost of treatment for chronic Hepatitis C, preventive and therapeutic vaccines against HCV are thus much, International conference
    Poster presentation

  • Development of therapeutic and preventive vaccines against hepatitis C virus
    Depeng Jiang, Suratno Lulut Ratnoglik, Aoki Chie, Deng Lin, Shoji Ikuo, Hotta Hak
    International Symposium on Hepatitis C Virus and Related Viruses, Oct. 2012, English, Organising Committee of the19th International Symposium on Hepatitis C Virus and Related Viruses, Venice, An estimated 170 to 200 million individuals are chronically infected with Hepatitis C virus (HCV) worldwide and 3 to 4 million individuals are newly infected each year. There is currently no vaccine available to protect against HCV. Considering the limited efficacy and high cost of treatment for chronic Hepatitis C, preventive and therapeutic vaccines against HCV are thus much, International conference
    Poster presentation

  • Identification of an E3 ubiquitin ligase that mediates ubiquitylation of hepatitis C virus NS5A protein
    Shoji Ikuo, Noriko Okada, Xiang Gan, Miho Makimoto, Chieko Matsui, Jang Da-Peng, Deng Lin, Yoshi-Hiro Ide, Hotta Hak
    第34回日本分子生物学会年会, Dec. 2011, Japanese, 日本分子生物学会, 横浜, Domestic conference
    Poster presentation

  • C型肝炎ウイルスによるGLUT2遺伝子発現抑制の分子機構
    松井千絵子, Shoji Ikuo, 兼田崇作, Deng Lin, 井出良浩, Hotta Hak
    第64 回日本細菌学会関西支部総会, Nov. 2011, Japanese, 第64 回日本細菌学会関西支部, 大阪, Domestic conference
    Oral presentation

  • C型肝炎ウイルスNS5Aの新規結合タンパク質であるヒストンメチル基転移酵素SMYD3の同定
    甘翔, Deng Lin, 陳明, 井出良浩, Shoji Ikuo, Hotta Hak
    第64 回日本細菌学会関西支部総会, Nov. 2011, Japanese, 第64 回日本細菌学会関西支部, 大阪, Domestic conference
    Oral presentation

  • C型肝炎ウイルスのNS3変異Y56/Q86及びコア蛋白変異Q70は高発癌性ウイルス株の指標となる
    El-ShamyA, Shoji Ikuo, 斎藤貴史, 西瀬雄子, 井出良浩, Deng Lin, 河田純男, Hotta Hak
    第15回日本肝臓学会大会, Oct. 2011, Japanese, 日本肝臓学会, 福岡, Domestic conference
    Poster presentation

  • Polymorphisms of serine protease-domain of NS3 and Core protein of hepatitis C virus genotype 1b associate with hepatocellular carcinoma development
    Ahmed El-Shamy, Shoji Ikuo, Takafumi Saito, Yoshi-Hiro Ide, Deng Lin, Sumio Kawata, Hotta Hak
    International Union of Microbiological Societies 2011 Congress, Sep. 2011, English, Federation of Microbiological Societies of Japan, 札幌, International conference
    Poster presentation

  • Molecular mechanisms involved in HCV infection-induced hepatic gluconeogenesis
    Deng Lin, Shoji Ikuo, Ogawa Wataru, Shusaku Kaneda, Tomoyoshi Soga, Da-peng Jiang, Yoshi-Hiro Ide, Hotta Hak
    International Union of Microbiological Societies 2011 Congress, Sep. 2011, English, Federation of Microbiological Societies of Japan, 札幌, International conference
    Poster presentation

  • Identification of an E3 ubiquitinin ligase that targets hepatitis C virus NS5A protein for ubiquitylation
    Shoji Ikuo, Noriko Okada, Xiang Gan, Shoji Miyagawa, Miho Makimoto, Ahmed El-Shamy, Deng Lin, Da-peng Jiang, Yoshi-Hiro Ide, Hotta Hak
    18th International Symposium on Hepatitis C Virus and Related Viruses, Sep. 2011, English, Organising Committee of the18th International Symposium on Hepatitis C Virus and Related Viruses, Seattle, U.S.A., International conference
    Poster presentation

  • Identification of an E3 ubiquitinin ligase that mediated ubiquitylation of hepatitis C virus NS5A protein
    Shoji Ikuo, Noriko Okada, Xiang Gan, Shoji Miyagawa, Miho Makimoto, Ahmed El-Shamy, Deng Lin, Da-peng Jiang, Yoshi-Hiro Ide, Hotta Hak
    International Union of Microbiological Societies 2011 Congress, Sep. 2011, English, Federation of Microbiological Societies of Japan, 札幌, International conference
    Oral presentation

  • Hepatitis C virus infection suppresses glucose transporter 2 gene expression by downregulation of hepatocyte nuclear factor 1α.
    Chieko Matsui, Shoji Ikuo, Shusaku Kaneda, Deng Lin, Da-peng Jiang, Yoshi-Hiro Ide, Hotta Hak
    International Union of Microbiological Societies 2011 Congress, Sep. 2011, English, Federation of Microbiological Societies of Japan, 札幌, International conference
    Poster presentation

  • Hepatitis C virus infection promotes hepatic gluconeogenesis through an NS5A-mediated, FoxO1-dependent pathway
    Deng Lin, Shoji Ikuo, Ogawa Wataru, Shusaku Kaneda, Tomoyoshi Soga, Da-peng Jiang, Yoshi-Hiro Ide, Hotta Hak
    18th International Symposium on Hepatitis C Virus and Related Viruses, Sep. 2011, English, Organising Committee of the18th International Symposium on Hepatitis C Virus and Related Viruses, Seattle, U.S.A., International conference
    Poster presentation

  • HCV-induced suppression of glucose transporter 2 gene expression via downregulation of hepatocyte nuclear factor 1α.
    Chieko Matsui, Shoji Ikuo, Shusaku Kaneda, Deng Lin, Da-peng Jiang, Yoshi-Hiro Ide, Hotta Hak
    18th International Symposium on Hepatitis C Virus and Related Viruses, Sep. 2011, English, Organising Committee of the18th International Symposium on Hepatitis C Virus and Related Viruses, Seattle, U.S.A., International conference
    Poster presentation

  • Development of hepatocellular carcinoma in NS3 transgenic mice
    Yoshi-Hiro Ide, Tatsuya Maebo, Chunying An, Da-peng Jiang, Deng Lin, Shoji Ikuo, Hotta Hak
    18th International Symposium on Hepatitis C Virus and Related Viruses, Sep. 2011, English, Organising Committee of the18th International Symposium on Hepatitis C Virus and Related Viruses, Seattle, U.S.A., International conference
    Poster presentation

  • C型肝炎ウイルスは酸化ストレスを介して糖新生を亢進し糖尿病発症に関与する
    Deng Lin, Shoji Ikuo, Hotta Hak
    第47回日本肝臓学会総会, Jun. 2011, Japanese, 日本肝臓学会, 東京, Domestic conference
    Oral presentation

  • 型肝炎ウイルスNS5Aに結合するユビキチンリガーゼの同定
    岡田典子, Shoji Ikuo, 甘翔, Deng Lin, Jiang Dapeng, 井出良浩, Hotta Hak
    第33回日本分子生物学会, Dec. 2010, Japanese, 日本分子生物学会, 神戸, Domestic conference
    Poster presentation

  • 慢性C型肝炎患者血清および非感染者血清を用いたＣ型肝炎ウイルス中和感受性決定部位の検討
    笹山美紀子, Shoji Ikuo, Adianti Myrna, 井出良浩, Jiang Dapeng, Deng Lin, Hotta Hak
    第58回日本ウイルス学会学術集会, Nov. 2010, Japanese, 日本ウイルス学会, 徳島, Domestic conference
    Poster presentation

  • 糖代謝に及ぼすC型肝炎ウイルスの影響及びその分子機序の解析
    Deng Lin, 兼田崇作, 井出良浩, Shoji Ikuo, Hotta Hak
    第58回日本ウイルス学会学術集会, Nov. 2010, Japanese, 日本ウイルス学会, 徳島, Domestic conference
    Oral presentation

  • HCVによる糖代謝障害の分子機序
    Shoji Ikuo, Deng Lin, Hotta Hak
    第58回日本ウイルス学会学術集会, Nov. 2010, Japanese, 日本ウイルス学会, 徳島, Domestic conference
    Public symposium

  • HCV genotype 2aおよび2bのNS5A多様性はペグインターフェロン/リバビリン併用療法の治療効果と相関する
    El-Shamy Ahmed, 金守良, 井出良浩, Deng Lin, Shoji Ikuo, Hotta Hak
    第58回日本ウイルス学会学術集会, Nov. 2010, Japanese, 日本ウイルス学会, 徳島, Domestic conference
    Oral presentation

  • C型肝炎ウイルス感染は転写因子FoxO1を介した糖新生を誘導する
    Deng Lin, 兼田祟作, 井出良浩, Shoji Ikuo, Hotta Hak
    第63回日本細菌学会関西支部総会, Nov. 2010, Japanese, 日本細菌学会関西支部, 大阪, Domestic conference
    Oral presentation

  • Sequence heterogeneity of NS5A of HCV genotypes 2a and 2b affects RVR and SVR to PEG-IFN/RBV combination therapy
    Ahmed El-Shamy, Soo-Ryang Kim, Yoshi-Hiro Ide, Deng Lin, Shoji Ikuo, Hotta Hak
    17th International meeting on hepatitis C virus and related viruses, Sep. 2010, English, Organising Committee of the17th International Meeting on Hepatitis C Virus and Related Viruses, Yokohama, Japan, International conference
    Poster presentation

  • Molecular mechanism of HCV-induced suppression of glucose transporter (GLUT) 2 expression
    Shoji Ikuo, Shusaku Kaneda, Deng Lin, Yoshi-Hiro Ide, Hotta Hak
    17th International meeting on hepatitis C virus and related viruses, Sep. 2010, English, Organising Committee of the17th International Meeting on Hepatitis C Virus and Related Viruses, Yokohama, Japan, International conference
    Poster presentation

  • Identification of an amino acid residue that determines sensitivity to virus neutralization by nonspecific inhibitors and specific neutralizing antibodies in human sera
    Mikiko Sasayama, Shoji Ikuo, Myrna Adianti, Yoshi-Hiro Ide, Deng Lin, Hotta Hak
    17th International meeting on hepatitis C virus and related viruses, Sep. 2010, English, Organising Committee of the17th International Meeting on Hepatitis C Virus and Related Viruses, Yokohama, Japan, International conference
    Poster presentation

  • HCV-induced generation of reactive oxygen species leads to Bax-mediated apoptosis through activation of the c-Jun NH2-terminal kinase signaling pathway
    Deng Lin, Yosi-Hiro Ide, Shoji Ikuo, Hotta Hak
    17th International meeting on hepatitis C virus and related viruses, Sep. 2010, English, Organising Committee of the17th International Meeting on Hepatitis C Virus and Related Viruses, Yokohama, Japan, International conference
    Poster presentation

  • C型肝炎ウイルスコア蛋白質の安定性調節因子E6AP及びPA28γの相互作用解析
    Deng Lin, Ide Yoshiharu, Hotta Hak, Shoji Ikuo
    第32回日本分子生物学会年会, Dec. 2009, Japanese, 日本分子生物学会, 横浜, Domestic conference
    Poster presentation

  • C型肝炎ウイルスNS5A蛋白質と相互作用する細胞性キナーゼの解析
    Ide Yoshiharu, Deng Lin, Shoji Ikuo, Hotta Hak
    第32回日本分子生物学会年会, Dec. 2009, Japanese, 日本分子生物学会, 横浜, Domestic conference
    Poster presentation

  • グルコーストランスポーターGLUT2の転写制御に及ぼすC型肝炎ウイルスの影響.
    Adachi Tetsuya, Deng Lin, Ide Yoshiharu, Shoji Ikuo, Hotta Hak
    第57回日本ウイルス学会学術集会, Oct. 2009, Japanese, 日本ウイルス学会, 東京, Domestic conference
    Poster presentation

  • Molecular mechanisms involved in HCV infection-associated predisposition of type 2 diabetes.
    Adachi Tetsuya, Deng Lin, Shoji Ikuo, Hotta Hak
    16th International symposium on hepatitis C virus and related viruses, Oct. 2009, English, Organising Committee of the16th International Meeting on Hepatitis C Virus and Related Viruses, ニース, フランス, International conference
    Oral presentation

  • C型肝炎ウイルス増殖に及ぼすエストラジオールの影響に関する検討.
    Adachi Tetsuya, Deng Lin, Ide Yoshiharu, Shoji Ikuo, Hotta Hak
    第57回日本ウイルス学会学術集会, Oct. 2009, Japanese, 日本ウイルス学会, 東京, Domestic conference
    Poster presentation

  • C型肝炎ウイルス感染によるインスリン抵抗性誘導の分子機序について.
    Ide Yoshiharu, Adachi Tetsuya, Deng Lin, Shoji Ikuo, Hotta Hak
    第57回日本ウイルス学会学術集会, Oct. 2009, Japanese, 日本ウイルス学会, 東京, Domestic conference
    Oral presentation

  • C型肝炎ウイルスによるBax活性化の分子機構の解析
    Deng Lin, Ide Yoshiharu, Shoji Ikuo, Hotta Hak
    第57回日本ウイルス学会学術集会, Oct. 2009, Japanese, 日本ウイルス学会, 東京, Domestic conference
    Oral presentation

  • Activation of JNK, but not p38 MAPK, is involved in HCV-induced, Bax-mediated apoptosis.
    Deng Lin, Shoji Ikuo, Hotta Hak
    16th International symposium on hepatitis C virus and related viruses, Oct. 2009, English, Organising Committee of the16th International Meeting on Hepatitis C Virus and Related Viruses, ニース, フランス, International conference
    Poster presentation

  • 高感染力価のHCV J6/JFH-1株の産生とウイルス細胞変性効果の解析
    Deng Lin, Nagano Motoko, Hotta Hak
    第60回日本細菌学会関西支部総会, Nov. 2007, Japanese, 日本細菌学会関西支部, 大阪, Domestic conference
    Oral presentation

  • Ｃ型肝炎ウイルス感染による細胞変性効果の分子機序の解析
    Deng Lin, Nagano Motoko, Hotta Hak
    第55回日本ウイルス学会学術集会, Oct. 2007, Japanese, 日本ウイルス学会, 札幌, Domestic conference
    Oral presentation

  • 高感染力価のHCV J6/JFH-1株の産生とウイルス細胞変性効果(CPE)の解析
    Deng Lin, Nagano Motoko, Hotta Hak
    第55回日本ウイルス学会学術集会, Oct. 2007, Japanese, 日本ウイルス学会, 札幌, Domestic conference
    Poster presentation

  • Hepatitis C virus infection induces apoptosis via a mitochondrial-related caspase pathway
    Deng Lin, Hotta Hak
    14thInternationalMeetingonHepatitisCVirusandRelatedViruses, Sep. 2007, English, Organising Committee of the14th International Meeting on Hepatitis C Virus and Related Viruses, グラスゴー, イギリス, International conference
    Poster presentation

  • HCV with high replication/release capacity in Huh-7.5 cell cultures obtained by a simple, rapid method exhibits two distinct types of cytopathic effect
    Deng Lin, Hotta Hak
    14thInternationalMeetingonHepatitisCVirusandRelatedViruses, Sep. 2007, English, Organising Committee of the14th International Meeting on Hepatitis C Virus and Related Viruses, グラスゴー, イギリス, International conference
    Poster presentation

  • The possible role for the NS5A and NS3/4A of hepatitis C virus in cell injury and hepatocarcinogenesis.
    HOTTA HAK, DENG LIN, NAGANO MOTOKO
    17th Asian Pacific Association for the study of the liver, Mar. 2007, English, Organising Committee of the 17th Asian Pacific Association for the study of the liver, 京都, International conference
    Oral presentation

■ Affiliated Academic Society
  • The Japanese Society for Virology
    Apr. 2003 - Present

■ Research Themes
  • Analysis of the effect of Nrf2-Prdx1 pathway on the degradation of hepatitis B virus RNA
    Lin Deng
    Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C), Grant-in-Aid for Scientific Research (C), Kobe University, Apr. 2021 - Mar. 2024, Principal investigator
    B型肝炎ウイルス(HBV)は、ヒト肝細胞に感染し、慢性肝炎、肝硬変、肝細胞癌などを含む肝疾患を引き起こすが、現時点において、根本的な治療法は確立されておらず、HBVを体内から完全に排除することは不可能とされている。本研究では、申請者が世界に先駆けて見出した、「HBVのXタンパク質 (HBx)の新規宿主結合因子Peroxiredoxin 1 (Prdx1)を介したHBV RNAの新規分解機構」のより詳細なメカニズムを明らかにすることにより、HBV関連疾患に対する新たな治療戦略シーズへの可能性を提示することを目的としている。 申請者は以前、Prdx1の発現を誘導する転写因子Nrf2の過剰発現がHBV増殖を有意に抑制することを見出している。そこで、令和3年度は、HBV感染によるNrf2-Prdx1経路の活性化の誘導機構について詳細に検討し、以下の成果を得た。(1) HBxタンパク質はNrf2タンパク質の安定化および核への移行を促進させることが明らかとなった。(2) 酸化ストレスセンサーであるKeap1はdouble-glycine repeat (DGR)ドメインを介してHBxと相互作用することが明らかとなった。(3) Nrf2はHBV core promoterに結合し、core promoter活性を阻害することが明らかとなった。以上のことから、HBV感染細胞において、Keap1はHBxと相互作用することにより、Nrf2の活性化を誘導し、活性化したNrf2はHBV core promoter活性を阻害することでHBV増殖を抑制すると考えられた。 これらの成果は、本研究の目的達成に向けた重要な知見であると考える。

  • 堀田 博
    学術研究助成基金助成金／基盤研究(C), Apr. 2012 - Mar. 2015
    Competitive research funding

  • DENG Lin, HOTTA Hak
    Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Kobe University, Apr. 2011 - Mar. 2014
    Hepatitis C Virus (HCV) NS5A is a multifunctional protein involved in HCV life cycle and HCV-induced liver pathologies. To elucidate the role of NS5A in HCV pathogenesis, we searched for host proteins interacting with NS5A by tandem affinity purification and identified a novel NS5A-interacting protein, SET and MYND domain-containing 3 (SMYD3), a histone methyltransferase involved in the proliferation of cancer cells. The interaction of NS5A with SMYD3 was confirmed by co-immunoprecipitation, proximity ligation assay, and confocal microscopy. NS5A predominately colocalized with SMYD3 in the cytoplasm. Moreover, the interaction between NS5A and SMYD3 transcriptionally activated AGR3, which is involved in breast, prostate and ovary tumorigenesis and belongs to the family of protein disulfide isomerases. Taken together, these data suggest that the interaction between NS5A and SMYD3 causes hepatocytic dysfunction through upregulation of AGR3 expression.
    Competitive research funding

  • DENG LIN
    Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Young Scientists (B), Kobe University, Apr. 2009 - Mar. 2011
    In this study, by using the J6/JFH1 strain of HCV and Huh7.5 cells, I demonstrated that HCV-induced ROS production triggers JNK activation, which leads to Bax activation and apoptosis. I also found that HCV core plays a role in HCV-induced apoptosis.
    Competitive research funding

  • DENG Lin
    Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Young Scientists (B), Kobe University, Apr. 2007 - Mar. 2009
    本研究では、HCV clone J6/JFH1株とHuh7.5細胞を用いて、HCV感染初期における肝細胞の細胞障害の分子機序について検討した。HCV感染により、ミトコンドリアにおける活性酸素種(ROS)の産生が増加し、アポトーシス促進タンパク質であるBaxの活性化及びBaxのミトコンドリアへの移行が亢進し、ミトコンドリア障害を介するcaspase-3依存的なアポトーシスが誘導されることを明らかにした。
    Competitive research funding

■ Academic Contribution Activities
  • Editorial Board Members for the Journal of Virology
    Editorial Board Members for the Journal of Virology
    2024 - 2026
    Peer review etc

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