Editorial Board Member

Fellowship (Human Genetics), McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, 2002 Postdoctoral Research Fellow, Howard Hughes Medical Institute (HHMI), Johns Hopkins Medical Institutions (JHMI), 2002 Ph.D. University of Florida, Biochemistry, Human Genetics, 1998 D.Sc. Chinese Academy of Sciences (CAS), 1991 The objectives of Dr. Zhang's lab is to elucidate molecular pathophysiology of vascular malformations, with emphasis on cerebral cavernous malformations (CCMs), microvascular malformations in the brain. Three genes have been identified as causes of CCMs; KRIT1 (CCM1), MGC4607 (CCM2), and PDCD10 (CCM3). All three CCM proteins interact with each other to form a CCM signaling complex (CSC) that, in turn, interacts with other cellular proteins. The main focus of his lab to define the role of CSC during angiogenesis, which has tremendous application for stroke, cancer biology, and vascular related diseases. Dr. Zhang's lab hypothesized that a CSC complex and their cellular partners coordinately regulates cellular signaling through their differentiated binding preferences and affinities in a spatiotemporal manner. By utilizing both in-vitro and in-vitro models, Dr. Zhang's previous work has established the importance of CSC in multiple endothelial cell signaling pathways. To fully address this critical question, his lab has been working to classify and establish their relationship among newly identified CSC cellular partners with proteomic, genomic and systems biology approaches.

Cerebral cavernous malformations (CCM), CCM pathogenesis, CCM signaling complex (CSC), blood brain barrier (BBB), biomarkers, membrane progesterone receptors (mPRs), CSC-mPRs-PRG (CmP).