Dual effects of hepatitis C virus Core protein on the transcription of cyclin-dependent kinase inhibitor p21 gene

H. J. Kwun, Kyung Lib Jang

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Transcription of p21 was activated in hepatitis C virus (HCV) Core-expressing HepG2 cells where its upstream p53 was stabilized. However, this effect was not absolutely required for the activation of p21 by Core, as demonstrated in Hep3B cells. In addition, an opposite effect on the transcription of p21 was observed in NIH3T3 and primary hepatocytes, where p53 was not decreased by Core. To explain the p53-independent regulation of p21 by Core, we identified a Core-responsive element between positions -74 and -83 of the p21 promoter, exactly overlapped with a tumour growth factor β (TGF-β)/butyrate responsive element. Furthermore, we demonstrated that Core could activate the p21 through the element by stimulating a butyrate pathway, whereas this was inhibited through a TGF-β pathway. The opposing effects of Core protein on the transcription of p21 might be important in understanding the progression of hepatic disease in HCV-positive patients.

Original languageEnglish (US)
Pages (from-to)249-255
Number of pages7
JournalJournal of Viral Hepatitis
Volume10
Issue number4
DOIs
StatePublished - Jul 1 2003

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Cyclin-Dependent Kinase Inhibitor p21
Butyrates
Hepacivirus
Intercellular Signaling Peptides and Proteins
Hep G2 Cells
Genes
Disease Progression
Hepatocytes
Neoplasms
Liver
Proteins
Hepatitis C virus nucleocapsid protein

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Infectious Diseases
  • Virology

Cite this

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abstract = "Transcription of p21 was activated in hepatitis C virus (HCV) Core-expressing HepG2 cells where its upstream p53 was stabilized. However, this effect was not absolutely required for the activation of p21 by Core, as demonstrated in Hep3B cells. In addition, an opposite effect on the transcription of p21 was observed in NIH3T3 and primary hepatocytes, where p53 was not decreased by Core. To explain the p53-independent regulation of p21 by Core, we identified a Core-responsive element between positions -74 and -83 of the p21 promoter, exactly overlapped with a tumour growth factor β (TGF-β)/butyrate responsive element. Furthermore, we demonstrated that Core could activate the p21 through the element by stimulating a butyrate pathway, whereas this was inhibited through a TGF-β pathway. The opposing effects of Core protein on the transcription of p21 might be important in understanding the progression of hepatic disease in HCV-positive patients.",
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Dual effects of hepatitis C virus Core protein on the transcription of cyclin-dependent kinase inhibitor p21 gene. / Kwun, H. J.; Jang, Kyung Lib.

In: Journal of Viral Hepatitis, Vol. 10, No. 4, 01.07.2003, p. 249-255.

Research output: Contribution to journalArticle

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