Inhibition of transcription elongation by the VHL tumor suppressor protein
| Autor: | Richard D. Klausner, Wilson H. Burgess, W. M. Linehan, K. P. Garrett, T. Aso, Joan W. Conaway, Arnim Pause, R. C. Conaway, D. R. Duan, De Chen |
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| Rok vydání: | 1995 |
| Předmět: |
von Hippel-Lindau Disease
Tumor suppressor gene Transcription Genetic endocrine system diseases Protein subunit Ubiquitin-Protein Ligases Elongin Molecular Sequence Data RNA polymerase II Elongin complex urologic and male genital diseases Cell Line Ligases Germline mutation Transcription (biology) Von Hippel–Lindau tumor suppressor Animals Humans Genes Tumor Suppressor Amino Acid Sequence Cloning Molecular Transcription factor neoplasms Multidisciplinary biology Tumor Suppressor Proteins Nuclear Proteins Molecular biology Recombinant Proteins female genital diseases and pregnancy complications Gene Expression Regulation Von Hippel-Lindau Tumor Suppressor Protein Mutation biology.protein RNA Polymerase II HeLa Cells Transcription Factors |
| Zdroj: | Scopus-Elsevier |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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