Richard Kew, Ph.D., Research Assistant Professor.
Richard R. Kew, Ph.D.
Assistant Professor of Pathology
Stony Brook University Medical Center
Stony Brook, NY 11794-8691
Tel: (631) 444-3941
Fax: (631) 444-3424
Email: rkew@notes.cc.sunysb.edu
Education:
| 1979 | B.S., Biological Sciences, University of Massachusetts at Lowell |
| 1981 | M.S., Biochemistry, University of Massachusetts at Lowell |
| 1986 | Ph.D., Cellular & Molecular Pathology, State University of New York at Stony Brook |
Postdoctoral Training:
| 1986-1988 | St. Louis University, St. Louis, MO |
| 1988-1990 | Graduate Hospital and the University of Pennsylvania, Philadelphia, PA |
Awards & Honors:
| 1979 |
Biological Sciences Senior Research Award, |
| 1989 | Recipient of a Hulda and George McKay Research Fellowship |
| 1991 | Recipient of the Young Investigator Award from the Society for Leukocyte Biology |
| 2000 | Leadership Award from the Heart Council of Long Island |
| 2005 | Promising Inventor Award from Research Foundation of SUNY |
| 2007 | Mentor Award from the University of Texas Medical School at Houston |
Research Summary:
Dr. Kew’s lab in interested in how components of the innate immune system contribute to the pathology of tissue injury. A major focus of the lab is to determine how plasma and cell-derived cofactors regulate chemotactic signals that direct leukocytes from the blood to sites of inflammation. Several experimental approaches (biochemical, cellular, molecular and proteomic) are being utilized to investigate the mechanisms by which a ubiquitous albumin-like plasma protein, the vitamin D binding protein (DBP), regulates leukocyte migration to activated complement peptide C5a. Aberrant and/or excessive activation of complement, with subsequent generation of C5a, has been strongly associated with the pathogenesis of several inflammatory disorders. C5a is one of the most potent and physiologically important chemotactic factors. Understanding how this activity is regulated will have major physiological significance and may facilitate the design of therapeutics that can modulate excessive tissue recruitment of leukocytes from the blood.
Selected Recent Publications (from a total of 44 peer-reviewed papers):
G. Trujillo and R.R. Kew. 2004. Platelet-derived thrombospondin-1 is necessary for the vitamin D binding protein (Gc–globulin) to function as a chemotactic cofactor for C5a.Journal of Immunology 173:4130-4136
Zhang, J. and R.R. Kew. 2004. Identification of a region of the vitamin D binding protein that mediates its C5a chemotactic cofactor function. Journal of Biological Chemistry 279:53282-53287.
McVoy, L.A. and R.R. Kew. 2005. CD44 and annexin A2 mediate the C5a chemotactic cofactor function of the vitamin D binding protein. Journal of Immunology 175:4754-4760.
Shah, A.B., S.J. DiMartino, G. Trujillo and R.R. Kew. 2006. Selective inhibition of the C5a chemotactic cofactor function of the vitamin D binding protein by 1,25(OH)2 vitamin D3. Molecular Immunology 43:1109-1115.
DiMartino, S.J., G. Trujillo, L.A. McVoy, J. Zhang and R.R. Kew. 2007. Upregulation of vitamin D binding protein (Gc-globulin) binding sites during neutrophil activation from a latent reservoir in azurophil granules. Molecular Immunology 44:2370-2377.
Last updated by andrea.schmidt on August 25, 2009