Paul S. Cooke
Professor and Chair
Department of Physiological Sciences
1333 Center Drive
Gainesville, FL 32610-0144
- BS Biology, Westminster College, Fulton, MO, 1978
- PhD Physiology, University of California, Berkeley, Berkeley, CA, 1983
Post-doctoral training, Reproductive biology, University of California, San Francisco, San Francisco, CA, 1984-1987
Honors and Awards
- Billie A. Field Endowed Chair in Reproductive Biology, Univ. of Illinois, 2004-2011
- Dr. Gordon and Mrs. Helen Kruger All-Around Excellence Award, Univ. of Illinois, 2004
- Pfizer Animal Health Award for Research Excellence, Univ. of Illinois, 2001
- Research Excellence Award, College of Veterinary Medicine, University of Illinois, 2000
- University Scholar, Univ. of Illinois, 1997-2000
- Young Andrologist Award, Am. Soc. of Andrology, 1996, Presented annually by Am. Soc. of Andrology to the outstanding U.S. scientist in male reproductive biology under 40 years old.
- The Levine Award for research excellence, Univ. of Illinois, 1993
- List of Teachers Ranked Excellent, Univ. of Illinois, 1988, 1989, 1991-1995, 1999-2001, 2005, 2007-2010
- National Research Service Award, National Institute of Health, 1984-1987
Dr. Cooke’s laboratory works in several areas of reproductive biology, and a recent key finding in the laboratory has been that spermatogonial stem cells from the testis can differentiate into a variety of other reproductive and non-reproductive cell types; this may have therapeutic implications for human medicine.
The laboratory also studies the development of uterine glands during the neonatal period, and specifically the ability of progesterone to inhibit or even halt development of these glands, which are essential for adult fertility. This work may provide a permanent, cost-effective, one-shot contraceptive strategy for some species.
Over 1 million people per year in the U.S. suffer a traumatic brain injury (TBI), and these is presently no effective therapy these injuries. The hormone progesterone has recently been shown to very significantly decrease mortality and morbidity in humans following TBI, but the molecular mechanism of this exciting therapeutic effect is unknown. Progesterone effects are mediated through a variety of nuclear and membrane receptors, and work is presently underway in the Cooke lab to determine which specific progesterone receptor(s) mediates the beneficial effects of this hormone in TBI and to determine whether progesterone acts through neurons or glia to produce its beneficial effect.
- Deficiency of CDKN1A or Both CDKN1A and CDKN1B Affect the Pubertal Development of Mouse Leydig Cells.
Additional publications here