Advisory Board

Dr. Jennifer Y. Zhang

The ScienceDaily article Skin Aging Reversed In Mice By Blocking Action Of Single Protein said

Researchers at the Stanford University School of Medicine have reversed the effects of aging on the skin of mice, at least for a short period, by blocking the action of a single critical protein.
The work could one day be useful in helping older people heal from an injury as quickly as they did when they were younger, said senior author Howard Chang, MD, PhD, assistant professor of dermatology. However, Chang and his colleagues warned their finding will likely be useful in short-term therapies in older people but not as a potential fountain of youth.
The work backs up the theory that aging is the result of specific genetic changes rather than accumulated wear and tear, Chang said. What’s more, those genetic changes can be reversed even late in life.
Other Stanford researchers who participated in the work are graduate student Tiara Kawahara and Jennifer Zhang, PhD, who was a postdoctoral scholar.

Jennifer Y. Zhang, Ph.D. is an Assistant Professor in the Department of Medicine, Division of Dermatology in Duke University. She earned her B.S. from Nankai University in China in 1990 and her PhD from the University of Florida in 1998. She has received postdoctoral training from the University of California at San Francisco and Stanford University.
Epidermis, the outermost layer of skin, is comprised of stratified epithelial cells and undergoes life-long self renewal through a tight balance of cell proliferation and programmed cell death. This balancing process is regulated by a complex array of transcription factors and their upstream signaling molecules. Jennifer and her group members at Duke University are interested in investigating 1) genetic regulatory mechanisms involved in epithelial proliferation, differentiation and aging, and 2) signaling networks in epidermal homeostasis and carcinogenesis.
NF-kB and AP1 represent two families of the well known gene regulatory proteins and have been indicated in a wide range of cellular processes. Recent studies from Jennifer’s group and her colleagues in Stanford University have indicated that NF-kB and AP1 regulate epidermal cell growth control in an opposing fashion with the former induces cell growth arrest and aging. Their current efforts are directed at: 1) characterization of cross-talk between the upstream signaling molecules of NF-kB and AP1 proteins in epidermal growth control, and 2) identification of AP1 down stream targets promoting epidermal proliferation, differentiation and senescence, a process linked to aging, as well as cancer.
Jennifer coauthored Motif module map reveals enforcement of aging by continual NF-kB activity, Tumor Necrosis Factor Receptor 1/c-Jun-NH2-Kinase Signaling Promotes Human Neoplasia, CDK4 regulation by TNFR1 and JNK is required for NF-kappaB-mediated epidermal growth control, Innate inhibition of adaptive immunity: Mycobacterium tuberculosis-induced IL-6 inhibits macrophage responses to IFN-gamma, Escaping G1 restraints on neoplasia — Cdk4 regulation by Ras and NF-kappa B, and SP75 is encoded by the DP87 gene and belongs to a family of modular Dictyostelium discoideum outer layer spore coat proteins.