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Bruton's tyrosine kinase

Bruton's tyrosine kinase, also known as tyrosine-protein kinase BTK, is a tyrosine kinase that is encoded by the BTK gene in humans. BTK plays a crucial role in B cell development.

Structure
BTK contains five different protein interaction domains. These domains include an amino terminal pleckstrin homology (PH) domain, a proline-rich TEC homology (TH) domain, SRC homology (SH) domains SH2 and SH3, as well as a protein kinase domain with tyrosine phosphorylation activity. Part of the TH domain is folded against the PH domain while the rest is intrinsically disordered. == Function ==
Function
BTK plays a crucial role in B cell development as it is required for transmitting signals from the pre-B cell receptor that forms after successful immunoglobulin heavy chain rearrangement. It also has a role in mast cell activation through the high-affinity IgE receptor. BTK contains a PH domain that binds phosphatidylinositol (3,4,5)-trisphosphate (PIP3). PIP3 binding induces BTK to phosphorylate phospholipase C (PLC), which in turn hydrolyzes PIP2, a phosphatidylinositol, into two second messengers, inositol triphosphate (IP3) and diacylglycerol (DAG), which then go on to modulate the activity of downstream proteins during B-cell signalling. == Clinical significance ==
Clinical significance
Mutations in the BTK gene are implicated in the primary immunodeficiency disease X-linked agammaglobulinemia (Bruton's agammaglobulinemia); sometimes abbreviated to XLA and selective IgM deficiency. Patients with XLA have normal pre-B cell populations in their bone marrow but these cells fail to mature and enter the circulation. The BTK gene is located on the X chromosome (Xq21.3-q22). At least 400 mutations of the BTK gene have been identified. Of these, at least 212 are considered to be disease-causing mutations. BTK is important for the survival and proliferation of leukemic B cells, which motivated efforts to develop BTK inhibitors as treatments for B cell malignancies such as mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL). As BTK is also linked to autoimmune disorders, recent efforts have sought to evaluate BTK inhibition as a therapeutic strategy for treatment of diseases such as multiple sclerosis (MS) and rheumatoid arthritis (RA). BTK inhibitors Approved drugs that inhibit BTK: • Acalabrutinib (Calquence), approved in October 2017 for relapsed mantle cell lymphoma and in October 2019 for Chronic lymphocytic leukemia (CLL) and Small lymphocytic lymphoma (SLL) • Ibrutinib (Imbruvica), a selective Bruton's tyrosine kinase inhibitor. • Orelabrutinib, approved in China for patients with mantle cell lymphoma (MCL) and chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), who have received at least one treatment in the past. • Pirtobrutinib (Jaypirca), a reversible (non-covalent) inhibitor of BTK, for mantle cell lymphoma. • Remibrutinib (Rhapsido), for chronic spontaneous urticariaRilzabrutinib (Wayrilza) approved for immune thrombocytopeniaTirabrutinib (Velexbru), approved in March 2020, in Japan, for the treatment of recurrent or refractory primary central nervous system lymphoma. • Zanubrutinib (Brukinsa) for mantle cell lymphoma, chronic lymphocytic leukemia (CLL), or small lymphocytic lymphoma (SLL). It can be taken by mouth. Various drugs that inhibit BTK are in clinical trials: • Phase 3: • Evobrutinib for multiple sclerosis. • Fenebrutinib (RG7845) for multiple sclerosis. • Tolebrutinib, for multiple sclerosis. • Phase 2: • ABBV-105 for systemic lupus erythematosus (SLE) • Fenebrutinib (GDC-0853) for rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis and chronic spontaneous urticaria. • Phase 1: • ElsubrutinibPoseltinib, for autoimmune diseases, under development by Hanmi Pharmaceutical and Lilly as of 2015 • Luxeptinib (CG-806), for CLL, SLL, non-Hodgkin lymphoma, acute myeloid leukaemia, and myelodysplastic syndromes (Phase I Trial; Phase I Trial). The inhibitor targets multiple kinase pathways, including BTK and FLT3. • NemtabrutinibSpebrutinib (AVL-292, CC-292) • Tirabrutinib, for non-Hodgkin lymphoma and/or CLL. Renamed GS-4059 and now in trial NCT02457598. • VecabrutinibBranebrutinibCatadegbrutinibBexobrutideg / BexodegbrutinibSunvozertinibAvitinib == Discovery ==
Discovery
Bruton's tyrosine kinase is named for Ogden Bruton, who first described XLA in 1952. Later studies in 1993 and 1994 reported the discovery of BTK (initially termed B cell progenitor kinase or BPK) and found that BTK levels are reduced in B cells from XLA patients. == Interactions ==
Interactions
Bruton's tyrosine kinase has been shown to interact with: • ARID3ABLNK (SLP-65), • CAV1, • GNAQ, • GTF2I, • PLCG2, • PRKD1, and • SH3BP5. == References ==
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