Current position: Distinguished Professor
Institution /Faculty /Department : Graduate Institute and Department of Microbiology, National Taiwan University
Shu-Chun Teng is a Professor in the Department of Microbiology at National Taiwan University. He received his B.S. in Chemistry from National Taiwan University and his Ph.D. in Biochemistry in 1997 for research carried out in the lab of Dr. Abram Gabrial at Rutgers University. In 2000, after three years of postdoctoral work at Princeton University with Dr. Virginia Zakian in Molecular Biology, he started his own lab where his research concerns aging, with a focus on telomeres, the ends of chromosomes. Shu-Chun Teng has made critical contributions in two areas of aging biology: telomere replication and protein folding. His lab used yeasts to study the molecular basis in aging by systematically identifying both enzymatic and structural components involved in stress response and aging pathways, and characterizing how these proteins work. They take advantage of the genetically tractable model organism yeast to approach these questions and use our findings in yeast to extend our studies in mammalian cells since the fundamental mechanisms of these pathways are preserved from yeast to human.
Parkinson's disease (PD) is a common neurodegenerative disorder with the pathological hallmark of a-synuclein aggregations. Dysregulation of a-synuclein homeostasis caused by aging, genetic, and environmental factors underlie the pathogenesis of PD. While chaperones are essential for proteostasis, whether modulation of co-chaperones may participate in PD formation has not been fully characterized. Here, we assessed the expression of several HSP70- or HSP90-related factors under various stresses and found that BAG5 expression is distinctively elevated in etoposide- or H2O2-treated SH-SY5Y cells. Stress-induced p53 binds to the BAG5 promoter directly to stimulate BAG5. Induced BAG5 binds a-synuclein and HSP70 in both cell cultures and brain lysates from PD patients. Overexpressed BAG5 reduces cellular HSP70-mediated refolding activity. Importantly, a-synuclein aggregation in SH-SY5Y cells requires BAG5. BAG5 expression is also detected in transgenic SNCA mutant mice and PD patients in a disease severity-dependent manner. Together, our data reveal a stress-induced p53-BAG5-HSP70 regulation that provides a potential therapeutic angle for PD.