Xiao-Ming Yin, Professor
MD, Shanhai Medical University, 1982
PhD, University of Texas Southwestern Medical Center, 1991
Email: xmyin@pitt.edu
A cell has four choices once it is born, including differentiation to perform a special function, proliferation to expand to a population of its kind, and senescence to stay cool for the good time to come. But perhaps the most important choice is to survive or to die. Cell dies when its mission is accomplished or for the benefits of the population. Cell struggles for survive to perform its function and to maintain the health of the organs, and the individuals. Premature death and unjustified survival can be a problem. The fundamental interest of our laboratory is to elucidate the molecular mechanism of cell survival and cell death in all aspects: Why and when does a cell die, what is the significance of cell death, what is the molecule mechanisms of cell death and the modes of cell death (apoptosis, autophagy or necrosis), and what is the relationship of cell survival/death with the other three choices of a cell's fate? We are not only focusing on the molecular and cellular aspects, but also the pathophysiological consequence using disease models. Our studies are currently in the context of cancer biology, tissue injury and metabolic stress, but are constantly changing and evolving with new and exciting directions ready to be pursued by new members. For additional information, please see http://path.upmc.edu/people/faculty/yin.html.
We are employing a very diverse array of technology and approaches in addressing these questions, including transgenic/knockout mice (more than 10 lines), sophisticated cell culture systems for primary cells and established cell lines, digital imaging (conventional, fluorescent, electronic, real time and time-lapsed) on animals, cells, DNA and protein molecules), biochemical fractionation and analysis of cellular and subcellular components, molecular cloning and protein expression, gene expression or knock-down with regular and viral means in cells and in animals. We are also collaborating with experts in systems biology, molecular modeling and high through-put technology. We believe a multi-facet approach is the best way to study interesting biological phenomena that are of medical significance.
Recent Publication
Kim, T-H, Y. Zhao, W.-X. Ding, J. N. Shin, X. He, Y.-W. Seo, J. Chen, H. Rabinowich, A. A. Amoscato and X.-M. Yin. Bid-cardiolipin interaction at mitochondrial contact site contributes to mitochondrial cristae reorganization and cytochrome c release. Mol Biol. Cell 15:3061-3072, 2004.
Ding, W-X, H.-M. Ni, D. DiFrancesca, D. B. Stolz and X.-M. Yin. Bid-dependent mitochondrial generation of oxygen radicals alters mitochondrial structures and functions following death receptor activation. Hepatology 40: 403-413, 2004.
Ding, W.-X. and X.-M. Yin. Dissection of the multiple mechanisms of TNF -induced apoptosis in liver injury. J. Cell. Mol. Med. 8(4): 445-454, 2004.
Li, B., H.-M. Ni, X. Chen, D. DiFrancesca and X.-M. Yin. Deletion of Bid impedes cell proliferation and hepatic carcinogenesis. American J. Path. 166:1523-1532, 2005.
Yin, X-M. Bid, a BH3-only multi-functional molecule, is at the cross road of life and death. Gene, 369: 7-19, 2006.
Chen, X, W-X, Ding, H-M. Ni, W. Gao, Y-H Shi, A. A. Gambotto, J. Fan, A.A. Beg and X-M. Yin. Bid-independent mitochondria activation in TNF -induced apoptosis and liver injury. Mol. Cell. Bio. 27 (2): 541-553, 2007.
Ding, W-X, H-M. Ni, W. Gao, Y-F. Hou, M. A Melan, X. Chen, D. B. Stolz, Z.-M. Shao and X-M. Yin. Differential effects of endoplasmic reticulum stress induced-autophagy on cell survival. J. Bio. Chem. 282: 4702-4710, 2007.
Ding, W-X, H-M. Ni, X. Chen, J. Yu, L. Zhang and X.-M. Yin. A coordinated action of Bax, PUMA and p53 promotes MG132-induced mitochondria activation and apoptosis in colon cancer cells. Mol. Cancer Ther., 6:1062-1069, 2007.
Feng, R, H.-M. Ni, S. Y. Wang, I. L. Tourkova, M.R. Shurin, H. Harada and X.-M. Yin. Cyanidin-3-rutinoside, a natural polyphenol antioxidant, selectively kills leukemic cells by induction of oxidative stress. J. Bio. Chem.,282: 13468-13476, 2007.
Ding, W-X, H-M. Ni, W. Gao, T. Yoshimori, D.B. Stolz, D. Ron and X-M. Yin. Linking of autophagy to ubiquitin proteasome system is important for the regulation of endoplasmic reticulum stress and cell viability. Amer. J. Path. 171: 513-524, 2007.
Zhao, Y, D. DiFrancesca, X. Wang, R. Zarnegar, G. Michalopoulos and X. M. Yin. Promotion of Fas-mediated Apoptosis in Type II Cells by High Doses of Hepatocyte Growth Factor Bypasses the Mitochondrial Requirement. J. Cell Physiol, 213: 556-563, 2007.
Ding, W-X, H-M. Ni and X-M. Yin. Absence of Bax Switched MG132-induced Apoptosis to Non-Apoptotic Cell Death that Could be Suppressed by Transcriptional or Translational Inhibition. Apoptosis 12: 2233-2244, 2007
Yin, X.-M. Bid. in Encyclopedia of Cancer (2nd Edition. Ed. by Manfred Schwab), Springer, 2007.
Ni, H-M., X. Chen, L. Chen, D. DiFrancesca, H. Harada and X-M. Yin. The impact of genetic background and Bid on the phenotype of Bcl-2 deficiency in mice. Apoptosis 13: 53-62, 2008
Gao, W, W-X. Ding, D. B. Stolz and X.-M. Yin. Macroautophagy induced by exogenously introduced calcium. Autophagy, 4(6): 1-8, 2008
Shi, Y-H., W.-X. Ding, J. Zhou, J.-Y. He, Y. Xu; A. Gambotto, H. Rabinowich, J. Fan and X.-M. Yin. Expression of X-linked inhibition-of-apoptosis protein in hepatocellular carcinoma promotes metastasis and predicts tumor recurrence. Hepatology, 48:497-507, 2008.
Ding, W-X and X.-M. Yin. Sorting, recognition and activation of the misfolded protein degradation pathways through autophagy and the proteasome. Autophagy 4(2): 141-150, 2008
Yin, X.-M. W-X. Ding and W. Gao. Autophagy in the liver. Hepatology 47:1773-1785, 2008
