Inhbb Knockout mouse models

Activin B, activin AB, and inhibin B all derive from the beta B subunit encoded by Inhbb, the mouse ortholog of human INHBB, which engages ActRIIA or ActRIIB with ALK4 and, distinctively, with ALK7 to activate SMAD2 and SMAD3, a receptor preference that separates activin B pharmacology from activin A. Nulls survive but display defective eyelid closure at birth alongside reproductive, placental, and pancreatic islet abnormalities, while inhibin B serves clinically as a Sertoli cell and ovarian reserve marker. Conditional deletion is the right tool for adult liver regeneration, beta-cell, and hepatic iron questions where the perinatal ocular phenotype would otherwise confound interpretation. Subunit-swap and patient variant knockins test ligand-specific receptor usage, and humanization supports antibody and ligand trap development. Inhba shares receptors and expression domains extensively, so compound Inhba and Inhbb conditional alleles, with a driver validated in the relevant lineage, prevent misreading redundancy as dispensability.

Whole body loss of Inhbb gives the clearest readout when the question is whether the gene is required at all. Follow up tissue work can still move to a conditional allele if lethality or compensation appears.