Bruton tyrosine kinase (BTK) (BTK)

Bruton tyrosine kinase (BTK) is a non-receptor tyrosine kinase of the Tec family that is essential for B-cell development and signaling [1, 2]. It is primarily expressed in B-lymphocytes and myeloid cells, where it mediates signaling downstream of the B-cell receptor (BCR) and various cytokine receptors [1]. This signaling cascade is vital for the survival, activation, and proliferation of B-cells [2]. Mutations in the BTK gene cause X-linked agammaglobulinemia (XLA), a condition where patients lack mature B-cells and antibodies [1, 4]. In the context of cancer, BTK is often constitutively active in B-cell malignancies like chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL), making it a prime therapeutic target [3, 4]. BTK inhibitors, such as ibrutinib and zanubrutinib, work by binding to the kinase domain to block its activity, thereby inducing apoptosis in malignant B-cells [3]. Additionally, BTK's role in myeloid cell signaling has led to its exploration as a target for autoimmune and inflammatory disorders [4].

Other names

Bone marrow tyrosine kinase gene in chromosome XAGMX1ATKBPKBruton agammaglobulinemia tyrosine kinaseTyrosine-protein kinase BTK

Inhibition of the kinase activity of BTK, typically through covalent or non-covalent binding to the ATP-binding pocket, which disrupts B-cell receptor (BCR) signaling pathways [3, 4].