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Blocking neddylation elicits antiviral effect against hepatitis B virus replication
CONCLUSION: The manipulation of the neddylation pathway can thus provide new tools interfering with HBV persistence as well as novel therapeutic strategies against chronic hepatitis B.PMID:34716866 | DOI:10.1007/s11033-021-06886-w
Source: Mol Biol Cell - October 30, 2021 Category: Molecular Biology Authors: Karima Abounouh Mohammad Enamul Hoque Kayesh Haya Altawalah Bouchra Kitab Shuko Murakami Shintaro Ogawa Yasuhito Tanaka Hind Dehbi Pascal Pineau Michinori Kohara Soumaya Benjelloun Kyoko Tsukiyama-Kohara Sayeh Ezzikouri Source Type: research

Ubiquitously specific protease 4 inhibitor-Vialinin A attenuates inflammation and fibrosis in S100-induced hepatitis mice through Rheb/mTOR signalling.
In conclusion, USP4 was significantly elevated in autoimmune hepatitis mice and Vialinin A reduced USP4 level and attenuate inflammation and fibrosis in the liver. The mechanism may be related to regulation of Rheb/mTOR signalling. PMID: 33295107 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - December 9, 2020 Category: Molecular Biology Authors: Xu J, Chen D, Jin L, Chen Z, Tu Y, Huang X, Xue F, Xu J, Chen M, Wang X, Chen Y Tags: J Cell Mol Med Source Type: research

HBx combined with AFB1 triggers hepatic steatosis via COX-2-mediated necrosome formation and mitochondrial dynamics disorder.
Abstract Hepatitis B virus (HBV) infection and aflatoxin B1 (AFB1) exposure have been recognized as independent risk factors for the occurrence and exacerbation of hepatic steatosis but their combined impacts and the potential mechanisms remain to be further elucidated. Here, we showed that exposure to AFB1 impaired mitochondrial dynamics and increased intracellular lipid droplets (LDs) in the liver of HBV-transgenic mice in vivo and the hepatitis B virus X protein (HBx)-expressing human hepatocytes both ex vivo and in vitro. HBx combined with AFB1 exposure also up-regulated receptor interaction protein 1 (RIP1), ...
Source: J Cell Mol Med - July 6, 2019 Category: Molecular Biology Authors: Chen YY, Lin Y, Han PY, Jiang S, Che L, He CY, Lin YC, Lin ZN Tags: J Cell Mol Med Source Type: research

Induction of Huh ‑7 cell apoptosis by HCV core proteins via CK1α‑p53‑Bid signaling pathway.
Induction of Huh‑7 cell apoptosis by HCV core proteins via CK1α‑p53‑Bid signaling pathway. Mol Med Rep. 2018 Apr 05;: Authors: Shen S, Li C, Dai M, Yan X Abstract Hepatitis C virus (HCV)‑infected liver cells sensitize host cells to tumor necrosis factor (TNF)‑related apoptosis‑inducing ligand (TRAIL)‑induced cell apoptosis; however, the precise mechanisms are unknown. In the present study, flow cytometry demonstrated that the Annexin V‑positive Huh‑7 cell number was higher in groups transfected with core proteins when compared with the pcDNA3.1 group. The mRNA and protein expression...
Source: Molecular Medicine Reports - April 6, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Hepatitis B virus X protein increases microRNA ‑21 expression and accelerates the development of hepatoma via the phosphatase and tensin homolog/phosphoinositide 3‑kinase/protein kinase B signaling pathway.
Hepatitis B virus X protein increases microRNA‑21 expression and accelerates the development of hepatoma via the phosphatase and tensin homolog/phosphoinositide 3‑kinase/protein kinase B signaling pathway. Mol Med Rep. 2017 Mar 23;: Authors: Hou Z, Quan J Abstract Hepatitis B virus (HBV) X protein (HBx) is a key regulatory protein that is involved in HBV infection, replication and carcinogenesis of hepatocellular carcinoma (HCC). The aim of the present study was to investigate the role of HBx in the progression and metastasis of liver cancer cells and to determine the underlying molecular mechanism...
Source: Molecular Medicine Reports - March 27, 2017 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Crosstalk between different family members: IL27 recapitulates IFN γ responses in HCC cells, but is inhibited by IL6-type cytokines
In this study, we show that IL27 induces STAT1 and STAT3 phosphorylation in 5 HCC lines and 3 different types of non-transformed liver cells. We were especially interested in the relevance of the IL27-induced STAT3 activation in liver cells. Thus, we compared the IL27 responses with those induced by IFNγ (STAT1-dominated response) or IL6-type cytokines (IL6, hyper-IL6 (hy-IL6) or OSM) (STAT3-dominated response) by microarray analysis and find that in HCC cells, IL27 induces an IFNγ-like, STAT1-dependent transcriptional response, but we do not find an effective STAT3-dependent response. Validation experiments corroborate ...
Source: Biochimica et Biophysica Acta (BBA) Molecular Cell Research - December 9, 2016 Category: Molecular Biology Source Type: research

STAT3‑regulated long non‑coding RNAs lnc‑7SK and lnc‑IGF2‑AS promote hepatitis C virus replication.
Authors: Xiong Y, Jia M, Yuan J, Zhang C, Zhu Y, Kuang X, Lan L, Wang X Abstract Long non‑coding RNAs (lncRNAs) are a class of RNAs that do not code protein but are important in diverse biological processes. In previous years, with the application of high‑throughput sequencing, a large number of lncRNAs associated with virus infections have been identified and intensively investigated, however, there are few studies examining the association between lncRNAs and HCV replication. Previous studies have demonstrated that signal transducer and activator of transcription 3 (STAT3) is activated by the hepatitis C vi...
Source: Molecular Medicine Reports - September 4, 2015 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Heterogeneous ribonucleoprotein K (hnRNP K) binds miR-122, a mature liver-specific microRNA required for hepatitis C virus replication.
Abstract Heterogeneous ribonucleoprotein K (hnRNP K) binds to the 5' untranslated region of the hepatitis C virus (HCV) and is required for HCV RNA replication. The hnRNP K binding site on HCV RNA overlaps with the sequence recognized by the liver-specific microRNA, miR-122. A proteome chip containing ~17,000 unique human proteins probed with miR-122 identified hnRNP K as one of the strong binding proteins. In vitro kinetic study showed hnRNP K binds miR-122 with a nanomolar dissociation constant, in which the short pyrimidine-rich residues in the central and 3' portion of the miR-122 were required for hnRNP K bin...
Source: Molecular and Cellular Proteomics : MCP - September 1, 2015 Category: Molecular Biology Authors: Fan B, Sutandy FX, Syu GD, Middleton S, Yi G, Lu KY, Chen CS, Kao CC Tags: Mol Cell Proteomics Source Type: research

Interferon alpha (IFNα)-induced TRIM22 interrupts HCV replication by ubiquitinating NS5A.
Abstract TRIM22, a tripartite-motif (TRIM) protein, is upregulated upon interferon alpha (IFNα) administration to hepatitis C virus (HCV)-infected patients. However, the physiological role of TRIM22 upregulation remains unclear. Here, we describe a potential antiviral function of TRIM22's targeting of the HCV NS5A protein. NS5A is important for HCV replication and for resistance to IFNα therapy. During the first 24 h following the initiation of IFNα treatment, upregulation of TRIM22 in the peripheral blood mononuclear cells (PBMCs) of HCV patients correlated with a decrease in viral titer. This phenomenon was ...
Source: Cellular and Molecular Immunology - February 16, 2015 Category: Molecular Biology Authors: Yang C, Zhao X, Sun D, Yang L, Chong C, Pan Y, Chi X, Gao Y, Wang M, Shi X, Sun H, Lv J, Gao Y, Zhong J, Niu J, Sun B Tags: Cell Mol Immunol Source Type: research

Emerging roles of interferon-stimulated genes in the innate immune response to hepatitis C virus infection.
Abstract Infection with hepatitis C virus (HCV), a major viral cause of chronic liver disease, frequently progresses to steatosis and cirrhosis, which can lead to hepatocellular carcinoma. HCV infection strongly induces host responses, such as the activation of the unfolded protein response, autophagy and the innate immune response. Upon HCV infection, the host induces the interferon (IFN)-mediated frontline defense to limit virus replication. Conversely, HCV employs diverse strategies to escape host innate immune surveillance. Type I IFN elicits its antiviral actions by inducing a wide array of IFN-stimulated gen...
Source: Cellular and Molecular Immunology - December 29, 2014 Category: Molecular Biology Authors: Wong M, Chen SS Tags: Cell Mol Immunol Source Type: research

Involvement of ERK pathway in interferon alpha-mediated antiviral activity against hepatitis C virus.
Abstract Interferon alpha (IFN-α) is the key component of the therapy for hepatitis C virus (HCV) infection. IFN-α exerts anti-HCV activity by targeting certain signaling pathways. Using infectious HCV culture system in human hepatoma Huh7.5.1 cells, we analyzed functional relevance of extracellular signal-regulated kinase (ERK) pathway for IFN-α-mediated anti-HCV activity. IFN-α treatment resulted in activation of ERK pathway by increasing phosphorylation of c-Raf, MEK, and ERK1/2 in Huh7.5.1 cells, whereas HCV impaired such activation. IFN-α-dependent ERK1/2 phosphorylation was blocked by MEK inhibitor U012...
Source: Cytokine - December 23, 2014 Category: Molecular Biology Authors: Zhao L, Wang W, Wang W, Ren H, Qi Z Tags: Cytokine Source Type: research

Stat3 signaling activation crosslinking of TGF-β1 in hepatic stellate cell exacerbates liver injury and fibrosis
Conclusion We provide a novel role of Stat3 cooperating TGF-β1 in activation and anti-apoptotic effect of HSCs. Stat3 worsens liver fibrosis through the up-regulation of TGF-β1 and fibrotic product expression.
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - November 13, 2014 Category: Molecular Biology Source Type: research

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