Stimulation of c-Rel transcriptional activity by PKA catalytic subunit beta.

Nuclear factor kappaB (NF-kappaB) is a eukaryotic transcription factor which responds to different extracellular signals. It is involved in immune response, inflammation, and cell proliferation. Increased expression of c-Rel (or its viral homolog v-Rel), one component of the NF-kappaB factors, induces tumorigenesis in different systems. The activity of NF-kappaB can be regulated by protein kinase A in a cAMP-independent manner. Our previous results showed that c-MYC induces the activity of by inducing the transcription of the gene encoding the duanyu1529 catalytic subunit beta Constitutive expression of in Rat1a cells induces their transformation. Here we show that CREB is unlikely to be a phosphorylation target of duanyu1529-Cbeta as characterized by different cell lines. Electrophoretic mobility shift assays showed that c-Rel is present as a significant component of the NF-kappaB factors in c-MYC overexpressing status. The transcriptional activity of c-Rel was significantly stimulated by Coactivators p300/CBP are at least partially responsible for the enhanced activation mediated by c-Rel and duanyu1529-Cbeta. Interaction between c-Rel and duanyu1529-Cbeta was demonstrated using coimmunoprecipitation assays. Immunoprecipitation-in vitro phosphorylation assays showed the direct phosphorylation of c-Rel by duanyu1529-Cbeta. These results indicate that c-Rel is a reasonable phosphorylation target of and that the transcriptional activity of c-Rel is stimulated by duanyu1529-Cbeta possibly through the interaction with p300/CBP.

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