Results Identification of TAB2 as an N-CoR-Interacting Molecule The activity of this APP complex supports the model of which the AICD can activate specific targets that may be relevant in development and neurodegeneration. Thus, a subset of NF-κB-regulated genes can be activated following export of the N-CoR corepressor complex directly by IL-1β or, alternatively, by sufficiently elevated levels of an AICD/Fe65/Tip60 complex in vivo. Activity of this Tip60 complex is not dependent on IL-1β but is dependent on the acetyltransferase function of Tip60. Interestingly, a second proposed Tip60 complex consisting of the AICD, Fe65, and Tip60 can dismiss the N-CoR corepressor complex in vivo. Nuclear export of the N-CoR/TAB2 complex, in response to IL-1β, is associated with recruitment of a Tip60-containing complex to the KAI1 promoter. The consequence of this IL-1β-dependent nuclear export is to relieve repression by a subset of N-CoR-dependent transcription factors. In this manuscript, we identify a specific N-CoR/TAB2/HDAC3 complex that exhibits IL-1β signal-dependent export from nucleus to cytoplasm, and we identify the tetraspanin KAI1/CD82 as a specific target for repression by this complex.
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