Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel

Oncogene. 1999 Nov 22;18(49):6925-37. doi: 10.1038/sj.onc.1203222.


The avian Rev-T retrovirus encodes the v-Rel oncoprotein, which is a member of the Rel/NF-kappaB transcription factor family. v-Rel induces a rapidly fatal lymphoma/leukemia in young birds, and v-Rel can transform and immortalize a variety of avian cell types in vitro. Although Rel/NF-kappaB transcription factors have been associated with oncogenesis in mammals, v-Rel is the only member of this family that is frankly oncogenic in animal model systems. The potent oncogenicity of v-Rel is the consequence of a number of mutations that have altered its activity and regulation: for example, certain mutations decrease its ability to be regulated by IkappaBalpha, change its DNA-binding site specificity, and endow it with new transactivation properties. The study of v-Rel will continue to increase our knowledge of how cellular Rel proteins contribute to oncogenesis by affecting cell growth, altering cell-cycle regulation, and blocking apoptosis. This review will discuss biological and molecular activities of v-Rel, with particular attention to how these activities relate to structure - function aspects of the Rel/NF-kappaB transcription factors.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Apoptosis
  • Cell Division
  • Cell Transformation, Neoplastic*
  • DNA / metabolism
  • Humans
  • Molecular Sequence Data
  • Mutation
  • Oncogene Proteins v-rel / analysis
  • Oncogene Proteins v-rel / chemistry
  • Oncogene Proteins v-rel / physiology*
  • Protein Processing, Post-Translational
  • Proto-Oncogene Proteins c-rel / analysis
  • Structure-Activity Relationship
  • Transcriptional Activation


  • Oncogene Proteins v-rel
  • Proto-Oncogene Proteins c-rel
  • DNA