Inhbc Conditional Knockout mouse models

Largely confined to hepatocytes, the mouse ortholog of human INHBC, Inhbc, encodes the activin beta C subunit whose homodimer, activin C, signals weakly, and whose principal documented activity is heterodimerization with beta A to divert that subunit away from bioactive activin A, effectively lowering SMAD2 and SMAD3 tone in liver and prostate. Nulls are viable without overt pathology, so the informative designs are combinatorial and gain of function rather than simple deletion: hepatocyte-directed overexpression knockins test the sequestration model directly, and conditional nulls become interpretable mainly under regenerative or injury challenge such as partial hepatectomy or hepatotoxin exposure. Humanized alleles support biochemical dissection of subunit pairing preference. Inhbe lies adjacent and is coexpressed in hepatocytes, so the locus demands care: design floxed alleles that leave neighboring regulatory elements intact, and generate compound Inhbc and Inhbe alleles when metabolic or liver injury readouts are primary.

Inhbc 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.