TAK1 was shown to participate in regulation of transcription by transforming growth factor-beta (TGF-beta). TAK1 is stimulated in response to TGF-beta and bone morphogenetic protein. These results suggest that TAK1 functions as a mediator in the signaling pathway of TGF-beta superfamily members. TAB1 and TAB2 are TAK1 binding proteins that may function as activators of the TAK1 (TGF-b activated kinase 1) MAPKKK in TGF-b signal transduction. TAB1-induced TAK1 activation promoted the dissociation of active forms of IKKa and IKK b from active TAK1, whereas the IKK mutants remained to interact with active TAK1. TNF-a activated endogenous TAK1, and the kinase-negative TAK1 acted as a dominant negative inhibitor against TNF-a-induced NF-kB activation. TAK1 was suggested to act as a regulatory kinase of IKKs.
Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.