Abstract
Bruton’s tyrosine kinase (BTK), a member of the Tec family of protein tyrosine kinases (PTKs), plays a vital and diverse function in many cellular processes. BTK is expressed throughout B cell development, widely participating in multiple signal pathways including PI3K, PLCγ, and PKC. Those pathways play critical functions in cell proliferation, development, differentiation, survival, and apoptosis. The expression of BTK is selectively down-regulated in T lymphocytes and plasma cells and the relative level of BTK expression may be modulated in different developmental populations of B cells. Mutations in the gene for BTK are responsible for X-linked agammaglobulinemia (XLA) in human and X-inked immunodeficiency (xid) in mice. Both of these diseases are characterized by blocks in B-cell development at multiple stages and impaired function of residual mature B cells. To date, more than 1252 mutations have been identified in human BTK gene associating with XLA. Targeting BTK has achieved remarkable efficacy in B cell malignancies, multiple myeloma and related bone disease. The present review discusses the recent data regarding the role of BTK in B cell development and its structure, regulation, functions, expression and mutations.
Highlights
Non-receptor protein tyrosine kinases are targets in the treatment of a number of diseases
This review has briefly summarized work defining the structure of Bruton’s tyrosine kinase (BTK), the range of signaling pathways potentially utilizing BTK, and the mutations leading to altered BTK function
In the last decade quite a lot has been learned about the events related to B cell antigen receptor (BCR) signaling, the precise role of BTK in this pathway remains poorly understood
Summary
Non-receptor protein tyrosine kinases are targets in the treatment of a number of diseases. Bruton’s tyrosine kinase (BTK) is by far the most studied member of Tec family and is mainly expressed in B cells [14]. It is expressed in myeloid, mast cells [15,16]. In 1993, several research groups discovered the new tyrosine kinase, BTK, which is mutated in a human X-linked agammaglobulinemia (XLA), as known as Bruton’s disease. This was the first evidence for the involvement of a protein tyrosine kinase related to the Src-family of oncogenic proteins in a human genetic disease. This review will cover the structure, functions, expression, and mutations of BTK
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