Ectopic expression of hepatitis C virus core protein differentially regulates nuclear transcription factors.

Article Details

Citation

Shrivastava A, Manna SK, Ray R, Aggarwal BB

Ectopic expression of hepatitis C virus core protein differentially regulates nuclear transcription factors.

J Virol. 1998 Dec;72(12):9722-8.

PubMed ID
9811706 [ View in PubMed
]
Abstract

The putative core protein of hepatitis C virus (HCV) regulates cellular growth and a number of cellular promoters. To further understand its effect, we investigated the role of the core protein in the endogenous regulation of two distinct transcription factors, nuclear factor-kappaB (NF-kappaB) and activating protein-1 (AP-1), and the related mitogen-activated protein kinase kinase (MAPKK) and c-Jun N-terminal kinase (JNK). Stable cell transfectants expressing the HCV core protein suppressed tumor necrosis factor (TNF)-induced NF-kappaB activation. Supershift analysis revealed that NF-kappaB consists of p50 and p65 subunits. This correlated with inhibition of the degradation of IkappaBalpha, the inhibitory subunit of NF-kappaB. The effect was not specific to TNF, as suppression in core protein-expressing cells was also observed in response to a number of other inflammatory agents known to activate NF-kappaB. In contrast to the effect on NF-kappaB, the HCV core protein constitutively activated AP-1, which correlated with the activation of JNK and MAPKK, which are known to regulate AP-1. These observations indicated that the core protein targets transcription factors known to be involved in the regulation of inflammatory responses and the immune system.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Genome polyproteinP26664Details