Transcription factor TFIIH components enhance the GR coactivator activity but not the cell cycle-arresting activity of the human immunodeficiency virus type-1 protein Vpr

Tomoshige Kino, Makoto Tsukamoto, George P. Chrousos

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The human immunodeficiency virus type-1 (HIV-1)-accessory protein Vpr interacts with and potentiates the activity of the glucocorticoid receptor (GR) and arrests the host cell cycle at the G2/M boundary. Here we report that three core components of the general transcription factor (TF) IIH, CDK7, Cyclin H, and MAT1, enhance Vpr's GR coactivator activity but inhibit its cell cycle-arresting function. A CDK7 mutant defective in kinase activity for the C-terminal tail of RNA polymerase II, which cannot form a functional TFIIH complex, did not enhance Vpr coactivator activity. Overexpression of all three TFIIH components and p300 cooperatively enhanced Vpr coactivator activity, whereas TFIIH overexpression did not potentiate the transcriptional activity of a Vpr mutant, which does not bind p300/CBP. These findings suggest that TFIIH participates in Vpr's GR coactivating activity, at a step beyond its interaction with p300/CBP.

Original languageEnglish
Pages (from-to)17-23
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume298
Issue number1
DOIs
Publication statusPublished - 1 Nov 2002

    Fingerprint

Keywords

  • CDK7
  • Cell cycle arrest
  • Coactivator
  • Cyclin H
  • MAT1

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this