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Dev Cell ; 23(3): 611-23, 2012 Sep 11.
Artigo em Inglês | MEDLINE | ID: mdl-22975329

RESUMO

The NF-κB transcription factor controls diverse biological processes. According to the classical model, NF-κB is retained in the cytoplasm of resting cells via binding to inhibitory, IκB proteins and translocates into the nucleus upon their ligand-induced degradation. Here we reveal that Sef, a known tumor suppressor and inhibitor of growth factor signaling, is a spatial regulator of NF-κB. Sef expression is regulated by the proinflammatory cytokines tumor necrosis factor and interleukin-1, and Sef specifically inhibits "classical" NF-κB (p50:p65) activation by these ligands. Like IκBs, Sef sequesters NF-κB in the cytoplasm of resting cells. However, contrary to IκBs, Sef continues to constrain NF-κB nuclear entry upon ligand stimulation. Accordingly, endogenous Sef knockdown markedly enhances stimulus-induced NF-κB nuclear translocation and consequent activity. This study establishes Sef as a feedback antagonist of proinflammatory cytokines and highlights its potential to regulate the crosstalk between proinflammatory cytokine receptors and receptor tyrosine kinases.


Assuntos
Citocinas/antagonistas & inibidores , Citocinas/metabolismo , Citoplasma/metabolismo , Inflamação , NF-kappa B/metabolismo , Receptores de Interleucina/metabolismo , Transdução de Sinais , Animais , Células Cultivadas , Células HEK293 , Células HeLa , Humanos , Camundongos , NF-kappa B/antagonistas & inibidores , Células NIH 3T3
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