Baisong Lu, PhD
Baisong Lu, Ph.D., Assistant Professor
Dr. Baisong Lu was born and raised in Hunan, a southern Province of China. He received his Bachelor’s Degree in biology from Beijing Normal University in 1991. He attended graduate school at Chinese PLA Medical Institute in molecular genetics in the same year. Upon graduation, he accepted a research position with Beijing Institute of Biotechnology. Since 2000 he received postdoctoral training at Harvard Medical School (2000) and Baylor College of Medicine (2000-2003). Then he ran his own lab as an associate professor at Beijing Institute of Biotechnology from 2003 to 2005. Beginning in January 2006 he worked as a Research Associate at Baylor College of Medicine. Shortly after that he joined the Wake Forest Institute for Regenerative Medicine as an Instructor. Dr. Lu is the author of more than twenty peer-reviewed papers and the inventor on a patent.
SYNOPSIS OF AREA OF INTEREST: Dr. Lu’s research interests include generating and using rodent models for the study of human reproduction-related and mitochondrial dysfunction-related diseases and conditions.
DETAILED AREA OF INTEREST:
1) Gene regulation of germ cell development: Germ cell development is a complicated and tightly regulated process. Dr. Lu is interested in defining the roles of genes involved in this process. He is involved in the determination of the
Pog/Fancl gene mutated in Germ Cell Deficient (gcd) mouse and the definition of its role in early germ cell development. His other works include the discovery of a novel male germ-cell specific gene network consisting of gametogenetin (Ggn), gametogenetin binding protein 1 (Ggnbp1), gametogenetin binding protein 2 (Ggnbp2), and ornithine decarboxylase antizyme 3 (Oaz3).
2) Mitochondrial dysfunction and mitochondria related human diseases: Dr. Lu is looking into the role and the mechanism of mitochondrial dysfunction in reproduction, erectile dysfunction and mitochondria related human diseases. The model he is working with is a transgenic mouse mutant with
Immp1l mutation and overdose mitochondrial superoxide generation.