BACKGROUND Bruton's Tyrosine Kinase (BTK) is member of the Tec family that is critically important for the growth, differentiation and activation of myeloid-, mast- and B-cells.1 BTK is activated firstly by membrane localization stimulated by PIP3 generation, and subsequently, by transphosphorylation of Tyr-551 by Src family kinases. Further activation occurs within the SH3 domain via a transphosphorylation mechanism. Tyr223 in this domain was phosphorylated by c-Abl.2 Activated BTK is involved in the phosphorylation of a number of signaling molecules involved in the PLCgamma, JNK and p38 MAPK pathways, leading to Ca2+ mobilization, mRNA stabilization and the induction of NF-kappaB and AP-1 transcription factors.3 BTK activity is negatively regulated by a number of proteins including inhibitor of BTK (IBTK), Sab and c-Cbl. Mutations in this enzyme are known in humans and result in the immunological disorder X-linked agammaglobulemia.4
1. Mohamed, A.J. et al: Immunol. Rev. 228:58-73, 2009
2. Backesjo, C.M. et al: Biochem. Biophy. Res. Commun. 299:510-5, 2002
3. Kurosaki, T & Hikida, M.: Immunol. Rev. 228:132-48, 2009
4. Toth, B. et al: Mol. Immunol. 46:2140-6, 2009
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