Jag2 Conditional Knockout mouse models

Jag2, the mouse ortholog of human JAG2, encodes a second Jagged-class Notch ligand and presents a DSL domain with EGF repeats to NOTCH1 through NOTCH3, triggering force-dependent ADAM10 and gamma-secretase processing and NICD-driven transcription with RBPJ and MAML. Its non-redundant requirements concentrate in thymic epithelium and gamma delta T cell development, the limb apical ectodermal ridge, tooth, and secondary palate, and nulls die perinatally with cleft palate, limb syndactyly, and thymic hypoplasia, while biallelic human variants cause a recessive muscular dystrophy tied to satellite cell Notch signaling. Given perinatal lethality, conditional deletion is the practical design for postnatal thymus, muscle regeneration, or skin work, patient missense knockins test whether variants impair surface presentation or receptor binding, and humanization supports antibody pharmacology. Jag1 overlaps substantially in epithelial and vascular contexts, so compound conditional alleles paired with a lineage-validated Cre driver prevent masked phenotypes.

Conditional deletion of Jag2 limits the genetic change to the lineage you choose. That helps in oncology, immunology, and metabolic work where systemic loss would muddy the read. After you confirm Cre specificity, crossing to Jag2 floxed stock yields usable cohorts.