Samir El-Dahr's Page

Samir S. El-Dahr, M.D.
Professor
Department of Pediatrics
Section of Pediatric Nephrology
Tulane University School of Medicine
1430 Tulane Avenue
New Orleans, LA 70012
Phone: 504 588-5377
Fax: 504 584-1852
e-mail: seldahr@tulane.edu

Education

M.D.   Aleppo University School of Medicine, Syria, 1982
Training in General Pediatrics.   Medical Center of Delaware, 1983-1986
Research Fellowship in Pediatric Nephrology.  University of Virginia, Charlottesville, 1986-90

Research Interests:


Recent Publications:

Marks J., Saifudeen Z., Dipp S., and El-Dahr S. S.  Two functionally divergent p53-responsive elements in the bradykinin B2 receptor promoter.  J. Biol. Chem. 278: 34158-34166, 2003.

Harrison-Bernard L.M., Dipp S., and El-Dahr S.S.  Renal and blood pressure phenotype in 18-mo-old bradykinin B2R(-/-)CRD mice.  Am. J. Physiol. 285: R782-R790, 2003.

Saifudeen Z., Marks J., Du H., and El-Dahr S. S.  Spatial repression of PCNA by p53 during kidney development.  Am. J. Physiol. 283: F727-F733, 2002.

Saifudeen, Z., Dipp, S. and El-Dahr S. S.  A role for p53 in terminal epithelial cell differentiation.  J. Clin. Invest 109: 1021-1030, 2002.

Prieto, M., Dipp, S., Meleg-Smith, S. and El-Dahr, S. S. (2001) Ureteric bud derivatives express angiotensinogen and AT1 receptors.  Physiol. Genomics. 6:29-37, 2001.

Yosipiv, I. V., Dipp, S. and El-Dahr, S. S. (2001). Targeted disruption of the bradykinin B2 receptor gene in mice alters the ontogeny of the renin-angiotensin system. Am. J. Physiol. (Renal Physiol). 281: F795-F801, 2001.

El-Dahr, S.S., Dipp, S., Meleg-Smith, S., Pinna-Parpaglia, P. and Madeddu, P.  Fetal ontogeny and role of metanephric bradykinin B2 receptors.  Pediatr. Nephrol.  14:288-296, 2000.

Saifudeen, Z., Du, H., Dipp, S. and El-Dahr, S. S..  The bradykinin type 2 receptor is a target for p53-mediated transcriptional activation.  J. Biol. Chem.  275:15557-155562, 2000.

El-Dahr, S. S., Harrison-Bernard, L. M., Dipp, S., Yosipiv, I. V. and Meleg-Smith, S.  Bradykinin B2 null mice are prone to renal dysplasia: gene-environment interactions in kidney development. Physiological Genomics 3:121-131, 2000.