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Honglin Li
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2300 Children's Plaza
no. 209 Room C321N
Chicago, IL 60614
Phone: (773) 755-6359
Fax: (773) 755-6344
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| Year |
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Degree |
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Institution |
| 1994 |
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Ph.D. |
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Wayne State University |
| 1988 |
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B.S. |
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University of Science and Technology of China |
Tong, X and Li, H (2004). eNOS protects from prostate cancer cells from TRAIL-induced apoptosis. Cancer Letters: 210, 63-71.
Ruffolo, S. C., Breckenridge, D. G., Nguyen, M., Goping, I. S., Gross, A., Korsmeyer, S. J., Li, H., Yuan, J., Shore, G. C. (2000). BID-dependent and BID-independent pathways for BAX insertion into mitochondria. Cell Death Differ: 7, 1101-1108.
Chou, J. J., Li, H., Salvesen, G., Yuan, J. and Wagner, G. (1999). Solution structure of Bid, an intracellular amplifier of apoptotic signaling. Cell: 96, 615-624.
Li, H., Zhu, H., Xu, C., Yuan, J. (1998). Cleavage of BID by caspase-8 mediates the mitochondrial damage in the Fas pathway of apoptosis. Cell: 94, 491-501.
Zhou, B-B., Li, H., Yuan, J., Kirschner, M. W. (1998). Caspase-dependent activation of cyclin-dependent kinases during Fas-induced apoptosis in Jurkat cells. Proc. Natl. Acad. Sci. USA : 95, 6786-6790.
Li, H., Bergeron, L., Cryns, V., Pasternack, M. S., Zhu, H., Shi, L., Greenberg, A., Yuan, J. (1997). Activation of caspase-2 in apoptosis. J. Biol. Chem. : 272, 21010-21017.
Li, H. and Nicholson, A. W. (1996). Defining the enzyme binding domain of a ribonuclease III processing signal. Ethylation interference and hydroxyl radical footprinting using catalytically inactive RNase III mutants. EMBO J.: 15, 1421-1433.
2001 - The Eleanor Clarke Research Scholar of Development Neurobiology Research
1996 - NIH Postdoctoral Research Service Award
Last Updated: Sep 8 2004 5:47PM
Back to Top Li lab is interested in identification and characterization of novel regulators of cell proliferation and cell death, two fundamental processes critical for tissue hemeostasis and animal development. Dysregulation of these processes leads to the pathogenesis of many human diseases including cancer and degenerative diseases. Finding of novel regulatory mechanisms may help to develop novel therapies for diseases. We recently identified a novel protein C53 as an important regulator of cell cycle progression and DNA damage-induced apoptosis. We found that depletion of C53 protein in cancer cells leads to cell cycle defects and cell death, while its overexpression sensitizes various cancer cells to both chemotherapeutic agents and irradiation. Our further study suggests that C53 may play a critical role in regulation of cell cycle checkpoint. Our finding implicates that C53 may represent a novel target in cancer therapy.
Honglin (Honglin Li) Li h-li2@northwestern.edu 2300 Children's Plaza no. 209 Room C321N Chicago, IL 60614 Phone: (773) 755-6359 Fax: (773) 755-6344 Education Year Degree Institution 1994 Ph.D. Wayne State University 1988 B.S. University of Science and Technology of China Recent Publications Tong, X and Li, H (2004). eNOS protects from prostate cancer cells from TRAIL-induced apoptosis. Cancer Letters: 210, 63-71. Ruffolo, S. C., Breckenridge, D. G., Nguyen, M., Goping, I. S., Gross, A., Korsmeyer, S. J., Li, H., Yuan, J., Shore, G. C. (2000). BID-dependent and BID-independent pathways for BAX insertion into mitochondria. Cell Death Differ: 7, 1101-1108. Chou, J. J., Li, H., Salvesen, G., Yuan, J. and Wagner, G. (1999). Solution structure of Bid, an intracellular amplifier of apoptotic signaling. Cell: 96, 615-624. Li, H., Zhu, H., Xu, C., Yuan, J. (1998). Cleavage of BID by caspase-8 mediates the mitochondrial damage in the Fas pathway of apoptosis. Cell: 94, 491-501. Zhou, B-B., Li, H., Yuan, J., Kirschner, M. W. (1998). Caspase-dependent activation of cyclin-dependent kinases during Fas-induced apoptosis in Jurkat cells. Proc. Natl. Acad. Sci. USA : 95, 6786-6790. Li, H., Bergeron, L., Cryns, V., Pasternack, M. S., Zhu, H., Shi, L., Greenberg, A., Yuan, J. (1997). Activation of caspase-2 in apoptosis. J. Biol. Chem. : 272, 21010-21017. Li, H. and Nicholson, A. W. (1996). Defining the enzyme binding domain of a ribonuclease III processing signal. Ethylation interference and hydroxyl radical footprinting using catalytically inactive RNase III mutants. EMBO J.: 15, 1421-1433. Awards/Honors 2001 - The Eleanor Clarke Research Scholar of Development Neurobiology Research 1996 - NIH Postdoctoral Research Service Award
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