Inhibition of transcription elongation by the VHL tumor suppressor protein

D. Roxanne Duan, Arnim Pause, Wilson H. Burgess, Teijiro Aso, David Y.T. Chen, Karla P. Garrett, Ronald C. Conaway, Joan W. Conaway, W. Marston Linehan, Richard D. Klausner

Research output: Contribution to journalArticlepeer-review

508 Scopus citations

Abstract

Germline mutations in the von Hippel-Lindau tumor suppressor gene (VHL) predispose individuals to a variety of tumors, including renal carcinoma, hemangioblastoma of the central nervous system, and pheochromocytoma. Here, a cellular transcription factor, Elongin (SIII), is identified as a functional target of the VHL protein. Elongin (SIII) is a heterotrimer consisting of a transcriptionally active subunit (A) and two regulatory subunits (B and C) that activate transcription elongation by RNA polymerase II. The VHL protein was shown to bind tightly and specifically to the Elongin B and C subunits and to inhibit Elongin (SIII) transcriptional activity in vitro. +These findings reveal a potentially important transcriptional regulatory network in which the VHL protein may play a key role.

Original languageEnglish (US)
Pages (from-to)1402-1406
Number of pages5
JournalScience
Volume269
Issue number5229
DOIs
StatePublished - 1995
Externally publishedYes

ASJC Scopus subject areas

  • General

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