Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel.
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.
Gilmore
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Biology Department, Boston University, 5 Cummington Street, Boston, Massachusetts, MA 02215-2406, USA.
D000595:Amino Acid Sequence; D000818:Animals; D017209:Apoptosis; D002455:Cell Division; D002471:Cell Transformation, Neoplastic; D004247:DNA / Q000378:metabolism; D006801:Humans; D008969:Molecular Sequence Data; D009154:Mutation; D020572:Oncogene Proteins v-rel / Q000032:analysis / Q000737:chemistry / Q000502:physiology*; D011499:Protein Processing, Post-Translational; D020569:Proto-Oncogene Proteins c-rel / Q000032:analysis; D013329:Structure-Activity Relationship; D015533:Transcriptional Activation
D020572:Oncogene Proteins v-rel; D020569:Proto-Oncogene Proteins c-rel; D004247:DNA