Peng Wang, PhD Email Peng Wang
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- Position
- ASSOCIATE PROFESSOR | Medicine, Endocrinology, Diabetes and Bone Disease
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- Language
- English
Dr. Peng Wang has worked in the field of cellular proliferation and cell death for 15 years. He has studied the cellular and molecular mechanisms of programmed cell death in cancer cells induced by anticancer drugs. He has identified and separated the nuclear function of the important tumor suppressor, p53, on apoptosis induced by DNA damaging agents. He also delineated the cross-talk between the intrinsic and extrinsic death pathways through transcriptional regulation, and the cross-talk between autophagy and apoptosis through caspase-mediated Beclin-1 cleavage. He has also contributed to understanding how microRNAs regulate cancer cell proliferation.
In the past two years, Dr. Wang has turned his focus to pancreatic beta cell proliferation. Using his background described above on cell death and proliferation signaling pathways, he is: 1) developing cell-based strategies for small molecular screens aimed at inducing human beta cell expansion and survival; 2) using molecular approaches to generate continuously growing human beta cell lines using lentiviral systems; and, 3) using shRNA RNA and related approaches to silence cell cycle inhibitors in human beta cells, with the goal of inducing sustained, regulatable, and safe proliferation in human beta cells.
Education
BS, Shenyang Agricultural University
PhD, Institute of Genetics and Developmental Biology, Chinese Academy of Science
Postdoc, University of Pittsburgh
Language
English
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Dr.Wang did not report having any of the following types of financial relationships with industry during 2018 and/or 2019: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
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