A postdoctoral position is available to study the role of G protein-coupled receptor (GPCR)- and beta-arrestin-dependent signaling pathways in type 2 diabetes and obesity. The project involves the generation and analysis of new mouse models which express novel classes of designer GPCRs in a cell-type specific fashion (J Wess. Trends Endocrin Metab 27, 600-603, 2016). The use of these designer GPCRs makes it possible to activate distinct G protein- or beta-arrestin-dependent signaling pathways in a conditional and reversible fashion. Additional novel mouse models that lack distinct GPCRs or downstream signaling molecules (e.g. beta-arrestins) in a cell-type specific fashion will also be generated and analyzed.
The primary focus of the work will be on how GPCRs and beta-arrestins regulate the function of fat, skeletal muscle, and pancreatic alpha/beta cells to maintain proper glucose homeostasis. Mice will be analyzed by physiological (metabolic), pharmacological, molecular, and biochemical techniques. The ultimate goal is to identify molecular pathways through which GPCRs and GPCR-associated proteins contribute to the pathophysiology of type 2 diabetes and obesity.
Background in mouse physiology/pharmacology, preferably fat, skeletal muscle, and alpha/beta cell biology, and experience with genetically modified mice is required. Basic molecular biological skills are also essential.
The tentative starting date is fall 2017. The salary and benefits are as per NIH regulations commensurate with experience.
Please send a cover letter with CV, bibliography, and names of three references (including e-mail addresses and telephone numbers) to:
For more information, contact:
Jurgen Wess, PhD
Chief, Molecular Signaling Section, LBC
National Institute of Diabetes and Digestive and Kidney Diseases
Building 8A, Room B1-A05
Bethesda, MD 20892, USA
Tel: (301) 402-3589
Fax: (301) 480-3447
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