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TNIK or TRAF2 and NCK interacting kinase is characterized by an N-terminal kinase domain and a C-terminal GCK domain that serves a regulatory function. TNIK is mainly expression in brain, heart, and spleen and it is a specific effector of RAP2 which regulate actin cytoskeleton. TNIK is autophosphorylated in a manner dependent upon lys54 in the ATP-binding pocket of its kinase domain and plays a main role in cytoskeleton regulation. TNIK has also been shown to phosphorylate gelsolin, the principal intracellular and extracellular actin-severing protein, in vitro. This and evidence from mutational studies suggest that TNIK functions in the regulation of the cytoskeleton.
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