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Title:
Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel | Oncogene
Description:
The avian Rev-T retrovirus encodes the v-Rel oncoprotein, which is a member of the Rel/NF-κB 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-κB 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 IκBα, 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-κB transcription factors.
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oncogene, virol, bose, cell, gilmore, biol, mol, enrietto, virology, temin, nature, gélinas, avian, vrel, access, natl, usa, dis, article, hannink, humphries, cancer, proc, acad, sci, chen, hrdlicková, rice, content, nfκb, kabrun, olson, zhang, bargmann, white, research, cookies, nehyba, res, witter, privacy, open, walker, capobianco, mosialos, gilden, lim, press, genes, data,
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nature portfolio permissions reprints rel/nf-κb transcription factors privacy policy 1981 nature 294 nature author information authors advertising scientific legacy social media retroviral oncoprotein v-rel literature research tobacco research research nf-κb pathway personal data rapidly fatal lymphoma/leukemia springerlink instant access nf-κb data protection permissions v-rel oncoprotein dna-binding site specificity altering cell-cycle regulation v-rel induces privacy multiple mutations contribute explore content subscription content 1999 gene expression li c-ch european economic area animal model systems institutional subscriptions read antigen receptor-activated bose jr hr min-min wan noori-daloii mr hr bose jr accepting optional cookies journals search log affecting cell growth v-rel article purchase manage preferences structure – function aspects elsevier science publishers b-cell lymphoma content article gilmore
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headline:Multiple mutations contribute to the oncogenicity of the retroviral oncoprotein v-Rel
description:The avian Rev-T retrovirus encodes the v-Rel oncoprotein, which is a member of the Rel/NF-κB 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-κB 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 IκBα, 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 structureâââfunction aspects of the Rel/NF-κB transcription factors.
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