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博后招聘(USA) University of Nebraska-Lincoln 已有1人參與
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Employer: University of Nebraska-Lincoln Date Posted: 11/29/2015 Application Deadline: Open Until Filled Job Description Seeking a Ph.D. graduate for a Post-Doctoral fellow position in the Su Lab, Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE, USA Research in Su Lab is focused on lipid and lipoprotein metabolism, mechanism of metabolic syndrome, with a particular emphasis on the role of microRNAs, ER and mitochondrial stress in obesity, fatty liver disease and insulin resistance. Research also pertains to eIF2-alpha kinase PKR, cAMP responsive signaling protein, CREBH, SREBP-Insigs and VLDL metabolism. Requirements include a Ph.D. in a relevant field, as well as relevant peer-reviewed molecular/cell biology publications. Strong research experience on microRNA study is a prerequisite plus hands on experience with mammalian cell culture and basic molecular/cellular techniques (ie, WB, IP/blot, PCR, construct preparation, cell transfection, IF, live imaging). Priority given to applicants with microRNA study in published work. Please send CV and contact information for 3 referees to Dr. Qiaozhu Su at qsu2@unl.edu. In your application, please indicate which of your publications demonstrate your hands on experience in the relevant microRNAs/ molecular/cell techniques. Su Lab Research Interests: An important goal of Su’s laboratory is to investigate the associations between cellular stress signaling, lipid/lipoprotein metabolism as well as the underlying molecular mechanisms responsible for metabolic syndrome, such as obesity and diabetes. Her program concerns three main areas: (1) To investigate the association between microRNAs and the eIF2 alpha kinases PKR in atherogenic diets induced obesity and insulin resistance. This project will study the cross-talk between mitochondrial stress and ER stress induced by high fat diets and their contributions to the onset of metabolic syndrome. (2) To elucidate the mechanisms responsible for hyperactivation of hepatic de novo lipogenesis in insulin resistant animal models by investigating the interplay between two transcription factors, SREBP and CREBH, and their association with adaptor proteins, Insig-1, Insig-2 and SCAP. (3) To determine the mechanisms responsible for overproduction of very low density lipoprotein (VLDL) in subjects with obesity and diabetes. This concern will be addressed by delineating the assembly and secretion of VLDL from liver and its lipolysis in the circulation system. Specific attention will be paid to the peroxisome proliferator-activated receptor family (PPAR alpha family, microsomal triglyceride transfer protein (MTP)) and kinases involved in mediating cellular stress signaling, including PKR and PERK, in cell culture systems (e.g. hepatocytes, fibroblasts and adipocytes) as well as in insulin-resistant animal models induced by genetic intervention and/or lipogenic diets. Contact: Dr. Qiaozhu Su Nutrition and Health Sciences University of Nebraska-Lincoln 316F Ruth Leverton Hall Lincoln, NE, 68583 |
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