Jun, the oncoprotein.
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.
Vogt
P K
PK
Department of Molecular and Experimental Medicine, The Scripps Reasearch Institute, 10550 North Torrey Pines Drive, La Jolla, California, CA 9203, USA.
D000818:Animals; D002471:Cell Transformation, Neoplastic; D016384:Consensus Sequence; D004268:DNA-Binding Proteins / Q000235:genetics; D019281:Dimerization; D051790:G-Box Binding Factors; D020869:Gene Expression Profiling; D009154:Mutation; D016759:Oncogene Protein p65(gag-jun) / Q000235:genetics / Q000502:physiology*; D016755:Proto-Oncogene Proteins c-jun / Q000235:genetics / Q000502:physiology*; D018808:Transcription Factor AP-1 / Q000235:genetics / Q000502:physiology; D014157:Transcription Factors / Q000235:genetics; D015533:Transcriptional Activation
D004268:DNA-Binding Proteins; D051790:G-Box Binding Factors; D016759:Oncogene Protein p65(gag-jun); D016755:Proto-Oncogene Proteins c-jun; D018808:Transcription Factor AP-1; D014157:Transcription Factors