Activation of endogenous type I IFN signaling contributes to persistent HCV infection. - Wikidata - awgldk - TriplyDB

Activation of endogenous type I IFN signaling contributes to persistent HCV infection.

Activation of endogenous type I IFN signaling contributes to persistent HCV infection.

http://www.wikidata.org/entity/Q38210107

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Targeting of type I interferon in systemic autoimmune diseases Induction of apoptosis in pancreatic cancer cells by vesicular stomatitis virus.Type III Interferon Induces Distinct SOCS1 Expression Pattern that Contributes to Delayed but Prolonged Activation of Jak/STAT Signaling Pathway: Implications for Treatment Non-Response in HCV Patients Suppression of USP18 Potentiates the Anti-HBV Activity of Interferon Alpha in HepG2.2.15 Cells via JAK/STAT Signaling.Frequencies of Circulating MAIT Cells Are Diminished in Chronic HCV, HIV and HCV/HIV Co-Infection and Do Not Recover during Therapy Multiple functions of USP18.Gene expression profile after knockdown of USP18 in Hepg2.2.15 cells.Insulin receptor substrate-4 interacts with ubiquitin-specific protease 18 to activate the Jak/STAT signaling pathway.Interplay between Janus Kinase/Signal Transducer and Activator of Transcription Signaling Activated by Type I Interferons and Viral Antagonism.Analysis of TLR7, SOCS1 and ISG15 immune genes expression in the peripheral blood of responder and non-responder patients with chronic Hepatitis C.

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P2860

Activation of endogenous type I IFN signaling contributes to persistent HCV infection.

http://www.wikidata.org/entity/Q38210107

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article científic

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article scientifique

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artikel ilmiah

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artículo científico

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Activation of endogenous type I IFN signaling contributes to persistent HCV infection.

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type

label

Activation of endogenous type I IFN signaling contributes to persistent HCV infection.

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prefLabel

Activation of endogenous type I IFN signaling contributes to persistent HCV infection.

@en

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Reviews in Medical Virology

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Activation of endogenous type I IFN signaling contributes to persistent HCV infection.

@en

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Bing Liu

http://www.w3.org/2001/XMLSchema#string

Chunhui Yang

http://www.w3.org/2001/XMLSchema#string

Limin Chen

http://www.w3.org/2001/XMLSchema#string

Peibin Zeng

http://www.w3.org/2001/XMLSchema#string

Shilin Li

http://www.w3.org/2001/XMLSchema#string

Xiaoqiong Duan

http://www.w3.org/2001/XMLSchema#string

Yujia Li

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P2860

Immune activation and inflammation in HIV-1 infection: causes and consequences

Viperin (cig5), an IFN-inducible antiviral protein directly induced by human cytomegalovirus

ISG15 inhibits Ebola VP40 VLP budding in an L-domain-dependent manner by blocking Nedd4 ligase activity

ISG15 modification of filamin B negatively regulates the type I interferon-induced JNK signalling pathway

ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response

Influenza B virus NS1 protein inhibits conjugation of the interferon (IFN)-induced ubiquitin-like ISG15 protein

Identification of interferon-stimulated gene 15 as an antiviral molecule during Sindbis virus infection in vivo.

Regulating intracellular antiviral defense and permissiveness to hepatitis C virus RNA replication through a cellular RNA helicase, RIG-I

The UbcH8 ubiquitin E2 enzyme is also the E2 enzyme for ISG15, an IFN-alpha/beta-induced ubiquitin-like protein

Interferon-inducible ubiquitin E2, Ubc8, is a conjugating enzyme for protein ISGylation

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332-342

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scholarly article

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10.1002/RMV.1795

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5

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24

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Ian D McGilvray

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2014-05-08T00:00:00Z

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262197170

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24806972

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