Yidong Bai, Ph.D., Assistant 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:
Li, Y., D'Aurelio, M., Deng, J. H., Park, J. S., Manfredi, G., Hu, P., Lu, J., and Bai, Y. (2007).
An assembled complex IV maintains the stability and activity of complex I in mammalian mitochondria.J Biol Chem. Jun 15;282(24):17557-62. Epub 2007 Apr 23.

Park, J. S., Li, Y. F., and Bai, Y. (2007). 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. May;1772(5):533-42. Epub 2007 Jan 26.

Y. Li, J. Park, J.H. Deng, and Y. Bai (2006)
Cytochrome c oxidase subunit IV is essential for assembly and respiratory function of the enzyme complex.J Bioenerg Biomembr. Dec;38(5-6):283-91.

Deng JH, Li Y, Park JS, Wu J, Hu P, Lechleiter J, Bai Y. (2006) Nuclear Suppression of Mitochondrial Defects in Cells without the ND6 Subunit.Mol Cell Biol. Feb;26(3):1077-86.

Bai Y, Park JS, Deng JH, Li Y, Hu P. (2005) Restoration of mitochondrial function in cells with complex I deficiency. Ann N Y Acad Sci. May;1042:25-35.

Song X, Deng JH, Liu CJ, Bai Y. (2005) Specific point mutations may not accumulate with aging in the mouse mitochondrial DNA control region.Gene. May 9;350(2):193-9. Epub Apr 9.

Saelim N, John LM, Wu J, Park JS, Bai Y, Camacho P, Lechleiter JD. (2004) Nontranscriptional modulation of intracellular Ca2+ signaling by ligand stimulated thyroid hormone receptor.J Cell Biol. Dec 6;167(5):915-24. Epub Nov 29.

Sullivan PG, Dragicevic NB, Deng JH, Bai Y, Dimayuga E, Ding Q, Chen Q, Bruce-Keller AJ, Keller JN. (2004) Proteasome inhibition alters neural mitochondrial homeostasis and mitochondria turnover. J Biol Chem. May 14;279(20):20699-707. Epub 2004 Jan 22.

Zhao H, Li R, Wang Q, Yan Q, Deng JH, Han D, Bai Y, Young WY, Guan MX. (2004) Maternally inherited aminoglycoside-induced and nonsyndromic deafness is associated with the novel C1494T mutation in the mitochondrial 12S rRNA gene in a large Chinese family. Am J Hum Genet. Jan;74(1):139-52. Epub 2003 Dec 12.

MORE ON YIDONG BAI'S RESEARCH:
Ellison Medical Foundation Award
Project Funded by the UMDF