Artigo Acesso aberto Revisado por pares

c-rel activates but v-rel suppresses transcription from kappa B sites.

1991; National Academy of Sciences; Volume: 88; Issue: 9 Linguagem: Inglês

10.1073/pnas.88.9.3715

ISSN

1091-6490

Autores

Jun‐ichiro Inoue, Lawrence D. Kerr, Lynn J. Ransone, Eyal Bengal, Tony Hunter, Inder M. Verma,

Tópico(s)

Immune Response and Inflammation

Resumo

We show that the product of the protooncogene c-rel is a constituent of an NF-kappa B-like complex that binds to the kappa B site originally identified in the enhancer of immunoglobulin kappa light chain gene. c-rel protein synthesized in bacteria binds to the kappa B site in a sequence-specific manner. The rel-kappa B complex can be disrupted by incubation with anti-rel antibodies. The rel protein can form oligomers. The c-rel protein can activate transcription from promoters containing kappa B sites; v-rel, on the other hand, suppresses the transcription of genes linked to kappa B sites. Thus, v-rel may interfere with the normal transcriptional machinery of the cell by acting as a dominant negative mutant.

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