Department of Cellular and Structural Biology

CSB Faculty

 

Yidong Bai, Ph.D.

Associate Professor

 

Columbia University, 1996

 

MED 221D
(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 and also regulate 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 the dynamics of the machinery for oxidative phosphorylation, the role of mitochondrial dysfunction in human diseases including cancer and aging process. various approaches are also explored in restoring the mitochondrial function in cells with mitochondrial deficiency.
Dr. Bai is the current COGS chair of CSB master program.

 

Course Director:
    Mitochondria and Apoptosis (INTD 6008)
    Animal Models (CSBL 6021)
Instructor:
    Obesity Module of Fundamentals of Biomedical Sciences (INTD 5000)
Recent Publications:
Li Y, D'Aurelio M, Deng JH, Park JS, Manfredi G, Hu P, Lu J, Bai Y. An assembled complex IV maintains the stability and activity of complex I in mammalian mitochondria. J Biol Chem. 2007 Jun 15;282(24):17557-62.

 

Park JS, Li YF, Bai Y. Yeast NDI1 improves oxidative phosphorylation capacity and increases protection against oxidative stress and cell death in cells carrying a Leber's hereditary optic neuropathy mutation. Biochim Biophys Acta. 2007 May;1772(5):533-42.

 

Lu J, Sharma LK, Bai Y. Implications of mitochondrial DNA mutations and mitochondrial dysfunction in tumorigenesis. Cell Res. 2009 Jul;19(7):802-15.

 

Sharma LK, Fang H, Liu J, Vartak R, Deng J, Bai Y. Mitochondrial respiratory complex I dysfunction promotes tumorigenesis through ROS alteration and AKT activation. Hum Mol Genet. 2011 Dec 1;20(23):4605-16.

 

Li H, Kumar Sharma L, Li Y, Hu P, Idowu A, Liu D, Lu J, Bai Y. Comparative bioenergetic study of neuronal and muscle mitochondria during aging. Free Radic Biol Med. 2013 Oct;63:30-40.

 

Representative Publications:
Deng JH, Li Y, Park JS, Wu J, Hu P, Lechleiter J, Bai Y. Nuclear suppression of mitochondrial defects in cells without the ND6 subunit. Mol Cell Biol. 2006 Feb;26(3):1077-86.

 

Park JS, Sharma LK, Li H, Xiang R, Holstein D, Wu J, Lechleiter J, Naylor SL, Deng JJ, Lu J, Bai Y. 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.

 

Li Y, Li HZ, Hu P, Deng J, Banoei MM, Sharma LK, Bai Y. Generation and bioenergetic analysis of cybrids containing mitochondrial DNA from mouse skeletal muscle during aging. Nucleic Acids Res. 2010 Apr;38(6):1913-21.