(Q27472897)

English

Subversion of Cell Signaling Pathways by Hepatitis C Virus Nonstructural 5A Protein via Interaction with Grb2 and P85 Phosphatidylinositol 3-Kinase

scientific article (publication date: September 2002)

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scholarly article

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Subversion of Cell Signaling Pathways by Hepatitis C Virus Nonstructural 5A Protein via Interaction with Grb2 and P85 Phosphatidylinositol 3-Kinase (English)

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Hepatitis C virus

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based on heuristic

inferred from title

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based on heuristic

inferred from title

8

object named as

Michael G Katze

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author name string

Yupeng He

1

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Haruhisa Nakao

2

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Seng-Lai Tan

3

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Stephen J Polyak

4

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Petra Neddermann

5

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Sangeetha Vijaysri

6

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Bertram L Jacobs

7

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publication date

September 2002

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Journal of Virology

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76

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18

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9207-17

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describes a project that uses

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Europe PubMed Central

11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC136456/fullTextXML

based on heuristic

inferred from PubMed Central ID database lookup

Hepatitis C virus nonstructural 5A protein induces interleukin-8, leading to partial inhibition of the interferon-induced antiviral response

1 reference

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21 March 2017

Regulation of mRNA Translation and Cellular Signaling by Hepatitis C Virus Nonstructural Protein NS5A

1 reference

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Antiapoptotic and oncogenic potentials of hepatitis C virus are linked to interferon resistance by viral repression of the PKR protein kinase

1 reference

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1 reference

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NS5A, a nonstructural protein of hepatitis C virus, binds growth factor receptor-bound protein 2 adaptor protein in a Src homology 3 domain/ligand-dependent manner and perturbs mitogenic signaling

1 reference

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Control of PKR protein kinase by hepatitis C virus nonstructural 5A protein: molecular mechanisms of kinase regulation

1 reference

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Evidence that hepatitis C virus resistance to interferon is mediated through repression of the PKR protein kinase by the nonstructural 5A protein

1 reference

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To interfere and to anti-interfere: the interplay between hepatitis C virus and interferon.

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HIV-1 Nef associated PAK and PI3-kinases stimulate Akt-independent Bad-phosphorylation to induce anti-apoptotic signals

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X protein of hepatitis B virus modulates cytokine and growth factor related signal transduction pathways during the course of viral infections and hepatocarcinogenesis

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1 reference

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The hepatitis B virus-X protein activates a phosphatidylinositol 3-kinase-dependent survival signaling cascade

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Latent membrane protein 2A-mediated effects on the phosphatidylinositol 3-Kinase/Akt pathway

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Epstein-Barr virus LMP2A transforms epithelial cells, inhibits cell differentiation, and activates Akt.

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Hepatitis C virus NS5A protein protects against TNF-alpha mediated apoptotic cell death

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Properties of the hepatitis C virus core protein: a structural protein that modulates cellular processes

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Phosphatidylinositol-3 kinase dependent pathways: the role in control of cell growth, survival, and malignant transformation.

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Differentiation stage-specific inhibition of the Raf-MEK-ERK pathway by Akt.

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Hepatitis C virus NS5A protein inhibits interferon antiviral activity, but the effects do not correlate with clinical response

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SH2/SH3 signaling proteins

1 reference

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Suppression of interferon-induced antiviral activity in cells expressing hepatitis C virus proteins

1 reference

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Repression of the PKR protein kinase by the hepatitis C virus NS5A protein: a potential mechanism of interferon resistance

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2 June 2018

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27 November 2018

Protein kinase B (c-Akt): a multifunctional mediator of phosphatidylinositol 3-kinase activation.

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27 November 2018

Viral proteins that regulate cellular signalling.

1 reference

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27 November 2018

1 reference

https://pubmed.ncbi.nlm.nih.gov/12186904

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Hepatocellular carcinoma

1 reference

https://pubmed.ncbi.nlm.nih.gov/12186904

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Molecular clones of hepatitis C virus: applications to animal models

1 reference

https://pubmed.ncbi.nlm.nih.gov/12186904

12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Identifiers

10.1128/JVI.76.18.9207-9217.2002

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

OpenCitations bibliographic resource ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

ResearchGate publication ID

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