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We are interested in the factors which cause obesity, the mechanisms by which this happens and how interventions in this pathway can alleviate obesity or its associated diseases.
Our group uses a variety of model systems including cell culture, yeast, flies and mice to understand the signaling and metabolic pathways which are involved in these processes. We then use modern molecular biology, genetic and pharmacological tools to manipulate and learn more about the physiology of obesity.
Our team is looking for a postdoctoral fellow for a NIH funded project on the role of mTORC1 in lipogenesis and adipogenesis. The overall focus of our lab is identifying the molecular mechanisms by which nutrient homeostasis is maintained or disrupted, especially in muscle, adipose and liver tissues especially in conditions such as obesity and type 2 diabetes. The selected fellow will join an active project in determining the mechanisms by which mTORC1 is able to regulate lipid metabolism. They will explore and characterize several novel animal models of disrupted nutrient sensing, and will gain experience in cutting edge metabolic and genetic techniques. Funding is available for this project for five years. For further information, please email Dave Bridges (email@example.com) with your curriculum vitae and a brief statement of your career goals.
Required Education: The candidate must have a recent doctorate in biological sciences.
Qualifications: A solid publication record, good communication skills and expertise in molecular biology and cell culture studies is required. Experience in handling animals and evaluating lipid and carbohydrate homeostasis would also be a benefit. The candidate will also have the ability to work both individually and as part of a team.
To apply please go to https://academic.uthsc.edu/postdoc/postdoctoral1.php?appid=7802.
Date Posted: July 14, 2015
and Lois Weisman.
Roles for PI(3,5)P2 in nutrient sensing through TORC1
Molecular Biology of the Cell
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and Alan Saltiel.
Metabolic Crosstalk: molecular links between glycogen and lipid metabolism in obesity.
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