Pik3cb Conditional Knockout mouse — mammary specific context

Encoding p110 beta, Pik3cb is the ortholog of human PIK3CB and is unique among class IA catalytic subunits in receiving direct input from G protein coupled receptors through G beta gamma and from RAC1 and CDC42, in addition to canonical p85 mediated recruitment by phosphotyrosine. That wiring makes it the principal PIP3 source in PTEN-deficient prostate and other tumors and a driver of integrin dependent platelet activation and arterial thrombosis. Germline deletion is embryonic lethal, so conditional nulls are the practical tool, and a kinase-dead knockin is especially informative because p110 beta retains kinase-independent scaffolding roles in clathrin-mediated endocytosis and nuclear DNA replication that a null would conflate with catalytic loss. Given the reciprocal dependence between p110 alpha and p110 beta after isoform-selective inhibition, endpoint dictates design: pair conditional Pik3cb loss with Pten deletion for tumor latency, and choose kinase-dead alleles when the question is catalysis versus scaffold.

Pik3cb conditional knockout mice carry a floxed allele so you delete function only where Cre is active. The germline allele stays intact until you cross to a tissue specific Cre. Labs reach for this design when a global knockout is lethal, when they need adult onset loss, or when regional redundancy hides a whole body phenotype. For mammary work, plan Cre specificity, reporter crosses, and baseline phenotyping before you scale.