Jun, the oncoprotein

Oncogene. 2001 Apr 30;20(19):2365-77. doi: 10.1038/sj.onc.1204443.

Abstract

Cellular Jun (c-Jun) and viral Jun (v-Jun) can induce oncogenic transformation. For this activity, c-Jun requires an upstream signal, delivered by the Jun N-terminal kinase (JNK). v-Jun does not interact with JNK; it is autonomous and constitutively active. v-Jun and c-Jun address overlapping but not identical sets of genes. Whether all genes essential for transformation reside within the overlap of the v-Jun and c-Jun target spectra remains to be determined. The search for transformation-relevant targets of Jun is moving into a new stage with the application of DNA microarrays technology. Genetic screens and functional tests remain a necessity for the identification of genes that control the oncogenic phenotype.

Publication types

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

MeSH terms

  • Animals
  • Cell Transformation, Neoplastic*
  • Consensus Sequence
  • DNA-Binding Proteins / genetics
  • Dimerization
  • G-Box Binding Factors
  • Gene Expression Profiling
  • Mutation
  • Oncogene Protein p65(gag-jun) / genetics
  • Oncogene Protein p65(gag-jun) / physiology*
  • Proto-Oncogene Proteins c-jun / genetics
  • Proto-Oncogene Proteins c-jun / physiology*
  • Transcription Factor AP-1 / genetics
  • Transcription Factor AP-1 / physiology
  • Transcription Factors / genetics
  • Transcriptional Activation

Substances

  • DNA-Binding Proteins
  • G-Box Binding Factors
  • Oncogene Protein p65(gag-jun)
  • Proto-Oncogene Proteins c-jun
  • Transcription Factor AP-1
  • Transcription Factors