ITK (IL-2-inducible T-cell kinase) EC 18.104.22.168 is a member of the Tec family of nonreceptor tyrosine kinases, which includes Bruton's tyrosine kinase. It is critical for the growth, differentiation and activation of T-cells. ITK is expressed in T-lymphocytes and acts downstream from T-cell receptor (TCR) stimulation. Activation of PI 3-kinase results in the accumulation of PIP3, which in turn leads to the recruitment of ITK to the membrane, its activation and subsequent autophosphorylation. Activated ITK interacts with and phosphorylates PLCγ, eventually leading to Ca2+ mobilization, transcription, cytokine release and actin reorganization.
ITK signaling is important in the protective response of the Th2 effector cells to infection, mediating the secretion of interleukins 4, 5, 10 and 13. The enzyme also has a role in the production of IL-17A by Th17 cells, which is essential for antimicrobial activity as well as being involved in autoimmune disorders. ITK is a target for research in multiple sclerosis, cancer (both hematological malignancies and solid tumors) and graft versus host disease.
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Literature for ITK
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