BBS Faculty Member - Jordan Kreidberg

Jordan Kreidberg

Department of Pediatrics

Boston Children's Hospital
Department of Urology, Enders 1060.1
300 Longwood Avenue
Boston, MA 02115 - 5737
Tel: 617-919-2959
Fax: 617-730-0129
Email: jordan.kreidberg@childrens.harvard.edu
Lab Members: 6 postdoctoral fellows



Our research focuses on how stem cell and progenitor populations in developing organs are regulated by signaling networks. Important areas of study include how transcription factors and chromatin modification proteins are involved in organ development. We also study how signaling networks important in developing organs are co-opted in disease.

We have taken a genome-wide approach to identifying targets of the Wilms’ tumor-1 transcription factor (WT1) using chromatin immunoprecipitation, from embryonic and mature kidneys. These studies have identified WT1 as a master regulator of a network of gene expression in the kidney, regulating the expression of other transcription factors important in the developing and adult kidney. In a highly differentiated cell known as the podocyte, WT1 regulates the expression of genes vital to carrying out filtration of the blood to preserve homeostasis. Current studies are aimed at understanding how WT1 regulation of gene expression changes in podocyte injury states that lead to chronic kidney disease.

Our studies on organ development are being extended to several disease models. Polycystic Kidney Disease (PKD) is one of the most common genetic diseases. We are investigating roles for integrins and receptor tyrosine kinases in the pathogenesis of PKD. These studies have identified a role for Wnt signaling in PKD that we are continuing to investigate.

We have also begun to investigate the molecular basis for common urological malformations that lead to kidney failure.



Last Update: 1/4/2017



Publications

For a complete listing of publications click here.

 


 

Pandey, P., Qin, S., Ho, J. Zhou, J. and Kreidberg, J.A. Systems biology approach to identify transcriptional reprogramming and microRNA targets during progression of Polycystic Kidney Disease. (In Press, BMC System Biology 2011 Apr 25;5:56. PMID: 21518438

Qin, S., Taglienti, M., Nauli, S.M., Contrino, L.,Takakura, A., Zhou, J. and Kreidberg, J.A. Failure to ubiquitinate c-Met leads to hyperactivation of mTOR signaling in a mouse model of autosomal dominant polycystic kidney disease J. Clinical Investigation 2010 120(10):3617-3628

Hartwig, S., Ho, J., Pandey, P., MacIsaac, K., Taglienti, M., Xiang, M., Alterovitz, G., Ramoni, M., Fraenkel. E., and Kreidberg, J.A. . Genomic Characterization of Wilms’ Tumor Suppressor-1 Targets in Nephron Progenitor Cells during Kidney Development. Development. 2010 137:1189-1203



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