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Binding of the von Hippel-Lindau tumor suppressor protein to Elongin B and C.

Science (New York, N.Y.) | Sep 8, 1995

http://www.ncbi.nlm.nih.gov/pubmed/7660130

Germ-line mutations of the von Hippel-Lindau tumor suppressor gene (VHL) predispose individuals to a variety of human tumors, and somatic mutations of this gene have been identified in sporadic renal cell carcinomas and cerebellar hemangioblastomas. Two transcriptional elongation factors, Elongin B and C, were shown to bind in vitro and in vivo to a short, colinear region of the VHL protein (pVHL) that is frequently mutated in human tumors. A peptide replica of this region inhibited binding of pVHL to Elongin B and C whereas a point-mutant derivative, corresponding to a naturally occurring VHL missense mutation, had no effect. These results suggest that the tumor suppression function of pVHL may be linked to its ability to bind to Elongin B and C.

Pubmed ID: 7660130 RIS Download

Mesh terms: Amino Acid Sequence | Animals | Carcinoma, Renal Cell | Genes, Tumor Suppressor | Germ-Line Mutation | Humans | Ligases | Mice | Molecular Sequence Data | Nuclear Proteins | Point Mutation | Recombinant Fusion Proteins | Transcription Factors | Transfection | Tumor Cells, Cultured | Tumor Suppressor Proteins | Ubiquitin-Protein Ligases | Von Hippel-Lindau Tumor Suppressor Protein | von Hippel-Lindau Disease

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