X-linked nephrogenic diabetes insipidus (XNDI) is a severe kidney disease caused by inactivating mutations in the V2 vasopressin receptor (V2R) gene, resulting in the loss of renal urine-concentrating ability. At present, no specific pharmacological therapy has been developed for the treatment of XNDI, primarily due to the lack of suitable animal models. We recently generated the first viable mouse model of XNDI in which the V2R gene can be conditionally deleted in adult mice.

A postdoctoral position is available to employ the newly generated V2R mutant mice as an animal model to identify new drugs useful for the treatment of XNDI. The project will involve in vitro work with isolated collecting duct tissues as well as acute and chronic drug administration studies in vivo. Kidney function will be monitored by standard physiological techniques. Moreover, changes in renal morphology will be studied in live mice via MRI. Background in renal physiology/pharmacology and experience with genetically modified mice is essential. Basic molecular biological and biochemical skills are also required.

Annual stipend: $ 50,000 per year

To apply, click on the button below, or send a cover letter with CV, bibliography, and names of three references (including e-mail addresses and telephone numbers) to jwess@helix.nih.gov.

For more information, contact:

Jurgen Wess, Ph.D.
Chief, Molecular Signaling Section, LBC
NIH-NIDDK
Building 8A, Room B1-A05
Bethesda, MD 20892, USA
Tel: (301) 402-3589
Fax: (301) 480-3447
E-mail: jwess@helix.nih.gov
Web: http://www2.niddk.nih.gov/NIDDKLabs/IntramuralFaculty/WessJBCrgen.htm

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