Over-Expression of TRPC6 via CRISPR Based Synergistic Activation Mediator in BMSCs Ameliorates Brain Injury in a Rat Model of Cerebral Ischemia/Reperfusion.
Deletion of TRPC6 Attenuates NMDA Receptor-Mediated Ca<sup>2+</sup> Entry and Ca<sup>2+</sup>-Induced Neurotoxicity Following Cerebral Ischemia and Oxygen-Glucose Deprivation.