A post-doctoral position is available in the Department of Physiology and Neurobiology at the University of Connecticut to study epigenetic regulation of energy metabolism and physiology in the context of human diseases. In particular, the laboratory investigates the role of microRNAs and epigenetic regulators in the development of non-alcoholic and alcoholic fatty liver disease, non-alcoholic steatohepatitis, liver fibrosis, and cholestasis. The goals of the projects are to unravel the molecular mechanisms and the physiological functions of microRNAs and the regulators in the pathogenesis of liver diseases. We employ a multidisciplinary approach integrating molecular biology, biochemistry, cell biology, genomics, and physiology to tackle the questions in genetically engineered mouse models and isolated cells.
We are seeking highly self-motivated and independent candidates with a Ph.D. in life sciences, biomedical sciences or a related field. Candidates with a strong background in metabolism, molecular biology, biochemistry, and cell biology are especially encouraged to apply. Expertise in epigenetic/transcriptional regulation, signal transduction, and inflammation is highly desired. Experience working with rodents is a plus. Ability to work both independently and collaboratively in a team, excellent communication skills, and critical thinking skills are desired.
To apply, please send a single PDF file containing your CV, a short statement of research experience and career goals (less than one page), and contact information of three references to Dr. Dong-Ju Shin by email: email@example.com. Review of applications will begin immediately and continue until the position is filled. Employment of the successful candidate will be contingent upon the successful completion of a pre-employment criminal background check.
The University of Connecticut is an Equal Opportunity/Affirmative Action Employer. All employees are subject to adherence to the State Code of Ethics which may be found at http://www.ct.gov/ethics/site/default.asp.
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