Chunxin (Black) Wang, Ph.D.

Headshot of Chunxin Wang

Chunxin (Black) Wang, Ph.D.

Staff Scientist
Address
Biochemistry Section

BG 35 RM 2C-1016
35 CONVENT DR
BETHESDA MD 20814

Dr. Chunxin Wang received B.S. in 1991, and M.S. in 1994, from Zhongshan (Sun Yat-sin) University, Guangzhou, China and his Ph.D. degree in 2004, from University of Maryland at College Park. His graduate studies, in the laboratory of Dr. Zhongchi Liu, were on the flower development of the model plant system, Arabidopsis thaliana, regarding the tso2 mutant (meaning ugly in Chinese), a gene encoding the small subunit of ribonucleotide reductase (RNR).

Following his graduate work, he joined Dr. Richard Youle’s lab at NIH/NINDS for postdoctoral research, focusing on the roles of Bax and Bak in apoptosis and Fis1 in mitochondrial dynamics. Dr. Wang was one of the few scientists who successfully generated human knockout cell lines via rAAV-based homolog recombination in late 2000s before the TALEN and CRISPR era. He was promoted to the Staff Scientist position in 2014. He currently investigates the molecular mechanisms of Parkin-dependent and independent mitophagy.

Mitophagy is a selective autophagy event to remove damaged mitochondria for quality control. While many human diseases are associated with mitochondrial dysfunctions, failure to remove dysfunctional mitochondria also contributes to neurological disorders. The two major recessive genes responsible for familiar Parkinson’s disease, Pink1 and Parkin play essential roles in mitophagy initiation. Whereas much has been studied on the upstream signaling events of mitophagy, downstream events of autophagy receptor recruitment are still not clear. In addition, Parkin-independent mitophagy also receives more attention recently due to its translational potentials. Dr. Wang’s research focuses on these two aspects to identify the essential factors in the pathways and investigate how autophagy machineries interact with each other and integrate all the signals to cooperatively complete the mitophagy process.