PI3KB

PI3KB refers to the catalytic subunit p110β of class I phosphoinositide 3-kinases (PI3Ks). In humans, it is encoded by the PIK3CB gene. p110β forms a lipid kinase complex with regulatory subunits of the p85 family and is expressed broadly across tissues. This enzyme phosphorylates phosphatidylinositol-4,5-bisphosphate (PIP2) to generate phosphatidylinositol-3,4,5-trisphosphate (PIP3) at the plasma membrane in response to signaling cues.

Activation of PI3KB can be driven by receptor tyrosine kinases as well as G protein–coupled receptor pathways, including inputs from Gβγ subunits. PIP3 serves as a docking site for pleckstrin homology (PH) domain–containing proteins such as AKT and PDK1, promoting AKT signaling and downstream pathways like mTOR. Regulation of PI3KB activity is balanced by phosphatases that remove PIP3, notably PTEN and SHIP family members.

Biological roles of PI3KB include control of cell growth, survival, metabolism, and cytoskeletal rearrangement, as well as contributions to platelet function and immune cell signaling. The enzyme participates in endocytosis and membrane trafficking, and its activity intersects with other PI3K isoforms in coordinating cellular responses.

Clinical significance varies with context. Alterations in PI3KB signaling can contribute to oncogenesis, and selective inhibitors of PI3Kβ have been explored for cancers, particularly those with PTEN deficiency, as well as inflammatory and thrombotic conditions. Inhibitor development aims to balance antitumor efficacy with potential metabolic and immunological side effects shared by PI3K inhibitors. Related isoforms include PIK3CA (p110α), PIK3CD (p110δ), and PIK3CG (p110γ).