Pik3cb (phosphatidylinositol 3-kinase, catalytic, beta polypeptide; also called p110β) is implicated in G-protein-coupled receptor (GPCR) signaling, PTEN-loss-driven cancers, and thrombocyte function. RAC1 and CDC42 (from the RHO subfamily of small GTPases) bind and activate PIK3CB via its RAS binding domain (RBD), but PIK3CB does not bind RAS.
S205D and K224A point mutations were introduced to the catalytic subunit of the mouse Pik3cb gene, disrupting interactions with Ras family GTPases. In vitro, the basal lipid kinase activity of purified recombinant protein is indistinguishable from
its wildtype counterpart. Cells from mice carrying mutations in the PIK3CB RBD show reduced phosphoinositide 3-kinase (PI3K) activity and defective chemotaxis. Mouse embryonic fibroblasts (MEFs) from these mice show reduced PI3K and these mice are resistant to bleomycin-induced lung fibrosis.
Homozygotes are smaller than their wildtype littermates both as newborns and as adults.
