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The research team uncovered a previously unknown role of a protein complex of STK24 and CCM3 in regulating the release of granules from neutrophils. The complex acted in a way that prevented the release of too many granules, which would acerbate tissue damage.
Senior author Dianqing Wu, professor of pharmacology, explains the implications of the study for stroke patients and those who have undergone tissue transplants. "This study provides potential new therapeutic targets to alleviate tissue damage during strokes and tissue transplantation," he said.
Wu added, "This study, by revealing the basic cellular function of CCM3, also points a new direction for the investigation of the pathogenic basis for Cerebral Cavernous Malformation (CCM) disease." CCM is a life-threatening neurovascular disease, which can be caused by mutations in CCM3.
Other authors are Yong Zhang, Wenwen Tang, Haifeng Zhang, Xiaofeng Niu, Yingke Xu, Jiasheng Zhang, Kun Gao, Titus Bobbon, Derek Toomre, and Wang Min of Yale School of Medicine; and Weijun Pan of the Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine.
To read the full study, visit the Developmental Cell website.
Source: Yale University