Is mig12 , a novel Opitz syndrome gene product partner , expressed in the embryonic ventral midline and co-operates with Mid1 to bundle and stabilize microtubules?
Our findings suggest that Mig12 co-operates with Mid1 to stabilize microtubules. Mid1-Mig12 complexes might be implicated in cellular processes that require microtubule stabilization, such as cell division and migration. Impairment in Mig12/Mid1-mediated microtubule dynamic regulation, during the development of embryonic midline, may cause the pathological signs observed in Opitz syndrome patients.
These results suggest that endothelial cPLA2α may play a principal role in L-NAME-induced hypertension and may be a target molecule for maintaining endothelial function under NO inhibition.