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

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


  • Kibel A
  • Iliopoulos O
  • DeCaprio JA
  • Kaelin WG


Science (New York, N.Y.)

Publication Data

September 8, 1995

Associated Grants


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