research Endothelial NMMHC IIA dissociation from PAR1 activates the CREB3/ARF4 signaling in thrombin-mediated intracerebral hemorrhage
In this study, the researchers reported that NMMHC IIA dissociates from PAR1 and activates the CREB3/ARF4 pathway, worsening thrombin-induced blood-brain barrier damage, suggesting it as a potential therapeutic target for blood-brain barrier-related diseases.

