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Inhibition of Transcription Elongation by the VHL Tumor Suppressor Protein
Ist Teil von
Science (American Association for the Advancement of Science), 1995-09, Vol.269 (5229), p.1402-1406
Ort / Verlag
Washington, DC: American Society for the Advancement of Science
Erscheinungsjahr
1995
Quelle
MEDLINE
Beschreibungen/Notizen
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.