Inhibition of transcription elongation by the VHL tumor suppressor protein.
Science
; 269(5229): 1402-6, 1995 Sep 08.
Article
em En
| MEDLINE
| ID: mdl-7660122
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.
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Base de dados:
MEDLINE
Assunto principal:
Fatores de Transcrição
/
Transcrição Gênica
/
Proteínas Nucleares
/
Genes Supressores de Tumor
/
Proteínas Supressoras de Tumor
/
Ubiquitina-Proteína Ligases
/
Doença de von Hippel-Lindau
/
Ligases
Tipo de estudo:
Prognostic_studies
Limite:
Animals
/
Humans
Idioma:
En
Ano de publicação:
1995
Tipo de documento:
Article