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Fanyun Kong

Researcher at Xuzhou Medical College

Publications -  41
Citations -  469

Fanyun Kong is an academic researcher from Xuzhou Medical College. The author has contributed to research in topics: Hepatitis B virus & Medicine. The author has an hindex of 9, co-authored 28 publications receiving 252 citations.

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MiR-409-3p and MiR-1896 co-operatively participate in IL-17-induced inflammatory cytokine production in astrocytes and pathogenesis of EAE mice via targeting SOCS3/STAT3 signaling.

TL;DR: It is elucidated that miR‐409‐3p and miR-1896, as co‐upregulated microRNAs in activated astrocytes and in EAE mice, targeted suppressor of cytokine signaling proteins 3 (SOCS3), which may be a therapeutic target for treating MS and neuroinflammation.
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Role of hepatitis B virus X protein in regulating LIM and SH3 protein 1 (LASP-1) expression to mediate proliferation and migration of hepatoma cells

TL;DR: Hepatitis B virus X protein (HBx) could upregulate LASP-1 through PI3-K pathway to promote the proliferation and migration of hepatoma cells and was demonstrated to be able to suppress hepatocellular cells proliferation and Migration.
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HBx activates FasL and mediates HepG2 cell apoptosis through MLK3-MKK7-JNKs signal module

TL;DR: HBx can induce HepG2 cell apoptosis via a novel active MLK3-MKK7-JNKs signaling module to upregulate FasL protein expression through inhibition of JNKs and activation of Fas/FasL proteins.
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The enhanced expression of death receptor 5 (DR5) mediated by HBV X protein through NF-kappaB pathway is associated with cell apoptosis induced by (TNF-α related apoptosis inducing ligand) TRAIL in hepatoma cells

TL;DR: It is demonstrated that increased apoptosis induced by TRAIL is associated with increased expression of DR5 that mediated by HBX through NF-κB pathway, providing a critical insight into the mechanism of hepatocyte apoptosis mediated byHBX in HBV infection.
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The interaction of hepatitis B virus with the ubiquitin proteasome system in viral replication and associated pathogenesis

TL;DR: A better understanding of the HBV-UPS interaction could provide novel insight into the mechanisms that are involved in viral replication and pathogenesis and help to develop potential treatment strategies targeting the UPS.