PIK3CB

p110β, the catalytic subunit encoded by PIK3CB, partners with p85-family regulatory subunits and is unique among class IA PI3Ks in responding to both receptor tyrosine kinases and G protein-coupled receptors, through its Ras-binding domain and interactions with Gβγ subunits. It generates PIP3 to activate AKT signaling and is the dominant isoform in PTEN-deficient tumors, where it sustains survival signaling after loss of the lipid phosphatase. p110β also contributes to insulin action, platelet function and neutrophil chemotaxis, features underpinning ongoing development of p110β-selective inhibitors for cancer and inflammatory indications. Compared with p110α, p110β activity is less dependent on input from oncogenic Ras, a distinction that shapes isoform-selective drug design.