Signal transduction by the JNK group of MAP kinases. COP9 signalosome: a multifunctional regulator of SCF and other cullin-based ubiquitin ligases. A new group of conserved coactivators that increase the specificity of AP-1 transcription factors. Revisiting the COP9 signalosome as a transcriptional regulator. CSN5 isopeptidase activity links COP9 signalosome activation to breast cancer progression. Genetic regulators of large-scale transcriptional signatures in cancer. Finally, we discuss about the dynamic equilibrium of the CSN complexes in regulation of the AP-1 pathway.Īdler, A.S., Lin, M., Horlings, H., Nuyten, D.S., van de Vijver, M.J., and Chang, H.Y. Thus, in contrast to CSN5/Jab1, which promotes AP-1 activity, CSN1 displays a negative effect on the AP-1 pathway. The decline in JNK1 is not caused by excessive proteolysis or by 3′ UTR-dependent mRNA instability, but by CSN1-dependent repression of one or multiple steps in transcriptional and posttranscriptional mechanisms. Further, CSN1 dramatically downregulates ectopic expression of c-Jun N-terminal kinase 1 (JNK1) in cultured cells. Here we show that CSN1 can inhibit phosphorylation of proto-oncogene c-Jun product and repress c-Jun dependent transcription. We have shown previously that CSN1 suppresses AP-1 transcription activity and inhibits ultraviolet (UV) and serum activation of c-fos expression. In addition, CSN associates with protein kinases and modulates cell signaling, particularly the activator protein 1 (AP-1) pathway. CSN regulates ubiquitinproteasome dependent protein degradation via the deneddylation and the associated deubiquitination activities. CSN1 is a component of the COP9 signalosome (CSN), a conserved protein complex with pleiotropic functions in many organs and cell types.
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