Hepatitis C viral proteins interact with Smad3 and differentially regulate TGF-beta/Smad3-mediated transcriptional activation (Q24302050)

transforming growth factor beta 1

GOA release 2020-03-11

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extrinsic apoptotic signaling pathway

GOA release 2020-03-11

1 reference

Efficient initiation of HCV RNA replication in cell culture

GOA release 2020-03-11

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Chi-Hong Chao

3

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author name string

Pei-Lin Cheng

series ordinal

1

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Meng-Hsiung Chang

series ordinal

2

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Yan-Hwa Wu Lee

series ordinal

4

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language of work or name

English

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publication date

14 October 2004

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published in

Oncogene

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volume

23

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page(s)

7821-38

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issue

47

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cites work

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Direct interaction of hepatitis C virus core protein with the cellular lymphotoxin-beta receptor modulates the signal pathway of the lymphotoxin-beta receptor

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Mechanisms for inhibition of hepatitis B virus gene expression and replication by hepatitis C virus core protein.

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Transforming growth factor beta induces the cyclin-dependent kinase inhibitor p21 through a p53-independent mechanism

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Transforming growth factor-beta gene expression in normal and fibrotic rat liver

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HPV16 E6 oncoprotein stimulates the transforming growth factor-beta 1 promoter in fibroblasts through a specific GC-rich sequence

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WAF1, a potential mediator of p53 tumor suppression

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Suppression of actinomycin D-induced apoptosis by the NS3 protein of hepatitis C virus

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Mutations increasing autoinhibition inactivate tumour suppressors Smad2 and Smad4.

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Distinct oligomeric states of SMAD proteins in the transforming growth factor-beta pathway

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Mechanism of E1A-induced transforming growth factor-beta (TGF-beta) resistance in mouse keratinocytes involves repression of TGF-beta type II receptor transcription

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Transmission of hepatitis C by intrahepatic inoculation with transcribed RNA

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Hepatitis C virus infection

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Human T-cell lymphotropic virus type 1 tax inhibits transforming growth factor-beta signaling by blocking the association of Smad proteins with Smad-binding element

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The human papilloma virus E7 oncoprotein inhibits transforming growth factor-beta signaling by blocking binding of the Smad complex to its target sequence

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Hepatitis C virus core protein represses the p21 promoter through inhibition of a TGF-beta pathway

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Hepatitis C virus core protein induces hepatic steatosis in transgenic mice

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E1A inhibits transforming growth factor-beta signaling through binding to Smad proteins

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Induction of apoptosis in cultured hepatocytes and in regressing liver by transforming growth factor beta 1

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Role of Smad proteins and transcription factor Sp1 in p21(Waf1/Cip1) regulation by transforming growth factor-beta.

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Inhibition of transforming growth factor beta signaling and Smad-dependent activation of transcription by the Latent Membrane Protein 1 of Epstein-Barr virus

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Hepatitis C virus core protein represses p21WAF1/Cip1/Sid1 promoter activity

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Transforming growth factor beta in hepatitis C virus infection: in vivo and in vitro findings

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Hepatitis B virus X protein inhibits transforming growth factor-beta -induced apoptosis through the activation of phosphatidylinositol 3-kinase pathway

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Interaction between hepatitis C virus proteins and host cell factors

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TGF beta signals through a heteromeric protein kinase receptor complex

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Cell transformation induced by hepatitis C virus NS3 serine protease

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Smad3 and Smad4 cooperate with c-Jun/c-Fos to mediate TGF-beta-induced transcription

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Receptor-associated Mad homologues synergize as effectors of the TGF-beta response

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