Mmp13 Conditional Knockout mouse models

Encoding collagenase 3, Mmp13 is the mouse ortholog of human MMP13 and the principal rodent interstitial collagenase, secreted as a zymogen activated by MMP2, MMP14, or plasmin and inhibited by TIMPs, with a catalytic domain that cleaves type I, II, and III collagen and a hemopexin domain that also permits degradation of aggrecan fragments, fibronectin, and perlecan. Transcription is driven by RUNX2, interleukin 1 beta, and MAPK signaling, and the enzyme is the dominant proteolytic driver of osteoarthritic cartilage loss as well as a required participant in growth plate remodeling and endochondral ossification, where compound loss with Mmp9 produces severe skeletal phenotypes. Design should therefore favor conditional deletion, using Col2a1-CreER or Acan-CreER for cartilage and osteoblast drivers for bone, rather than germline nulls that confound development with disease. Catalytically inactive knockins separate proteolysis from other functions, and humanization supports selective inhibitor testing where MMP1 cross-reactivity is the liability.

Conditional deletion of Mmp13 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 Mmp13 floxed stock yields usable cohorts.