CSB Faculty
Yidong Bai, Ph.D.
Associate Professor
Columbia University, 1996
(210) 567-0561
BAIY@UTHSCSA.EDU
We are interested in a comprehensive understanding of mitochondrial function at the molecular, cellular, tissue, and animal levels.
Mitochondria play a central role in cellular energy metabolism through the generation of ATP from oxidative phosphorylation. Mitochondria contain their own genomes and have a distinct molecular mechanism governing their gene expression and function.
Recent developments have also shown functional mitochondria are important in the regulation of apoptosis, signal transduction and cell growth. Mitochondrial defects have been reported in a wide range of conditions, such as diabetes, neurodegenerative diseases, cancers, and aging.
The central theme in the laboratory is to investigate the regulatory mechanisms working in mitochondria and the role of mitochondria in regulating various cellular pathways. In particular, we are interested in pathogenic mtDNA mutations associated with human diseases including cancer and aging process. Different approaches are utilized in restoring the mitochondrial function in cells with mitochondrial deficiency.
PUBLICATIONS:
Sharma LK, Lu J, Bai Y. (2009)
Mitochondrial respiratory complex I: structure, function and implication in human diseases. Curr Med Chem. 2009;16(10):1266-77.
Cai XY, Wang XF, Li SL, Qian J, Qian DG, Chen F, Yang YJ, Yuan ZY, Xu J, Bai Y, Yu SZ, Jin L. (2009) Association of mitochondrial DNA haplogroups with exceptional longevity in a Chinese population. PLoS One. 2009 Jul 29;4(7):e6423.
Lu J, Sharma LK, Bai Y. (2009) Implications of mitochondrial DNA mutations and mitochondrial dysfunction in tumorigenesis. Cell Res. 2009 Jul;19(7):802-15.
Ding Z, Ji J, Chen G, Fang H, Yan S, Shen L, Wei J, Yang K, Lu J, Bai Y. (2009) Analysis of mitochondrial DNA mutations in D-loop region in thyroid lesions. Biochim Biophys Acta. 2009 May 20.
Park JS, Sharma LK, Li HZ, Xiang R, Holstein D, Wu J, Lechleiter J, Naylor SL, Deng J, Lu J, Bai Y. (2009)
A heteroplasmic, not homoplasmic, mitochondrial DNA mutation promotes tumorigenesis via alteration in reactive oxygen species generation and apoptosis. Hum Mol Genet. 2009 May 1;18(9):1578-89.
MORE ON YIDONG BAI'S RESEARCH:
Ellison Medical Foundation Award
Project Funded by the UMDF
