Mab2l12 is highly conserved across species and has been implicated in various developmental processes, including eye and heart development. Human patients and transgenic mice with MAB21L2(R51C) mutation have severe skeletal anomalies in their appendicular skeleton. In this study, we aimed to investigate the specific impact of Mab2l12 in limb development. By conditional gene knockout model, we found that removing Mab21l2 by Prx1-cre during early limb development led to malformation of the stylopods. Histological examination revealed a three-day delay of endochondral ossification in the Prx1-cre
Mab21l2