Overview:

BTK (also known as Bruton tyrosine kinase) plays a crucial role in B-lymphocyte differentiation and activation. BTK interacts with SRC homology 3 domains of FYN, LYN and HCK that are activated upon stimulation of B- and T-cell receptors (1). Defects in the BTK gene cause Agammaglobulinemia, an X-linked immunodeficiency characterized by failure to produce mature B lymphocyte cells and associated with a failure of Ig heavy chain rearrangement. The unique role of BTK makes it a desirable target for potential anti-cancer, anti-inflammatory and anti-viral agents as well as other treatments (2).

Gene Aliases:

AT; ATK; BPK; XLA; IMD1; AGMX1; PSCTK

Genbank Number:

NM_000061

References:

1. Cheng, G. et al: Binding of Bruton's tyrosine kinase to Fyn, Lyn, or Hck through a Src homology 3 domain-mediated interaction. Proc. Nat. Acad. Sci. 91: 8152-8155, 1994.

2. Vassilev, A O. et al: Therapeutic potential of inhibiting Bruton's tyrosine kinase, (BTK). Curr Pharm Des. 2004;10(15):1757-66.