Associate Research Scientist

3 weeks ago

New York, United States Columbia University Full time

Associate Research Scientist - Molecular Medicine

Columbia University's Department of Medicine invites applications for a research position in the rank of Associate Research Scientist at The Columbia University Irving Medical Center in the Division of Molecular Medicine in the Laboratory of Dr. Ira Tabas. The position includes both laboratory and translational research.

Our laboratory studies the cellular biology of cardiometabolic disease, with an emphasis on the molecular-cellular mechanisms of non-alcoholic steatohepatitis (NASH) in obesity, advanced atherosclerosis, and hepatic insulin resistance and , and the links between these processes. We are seeking a talented Associate Research Scientist with interest and expertise in molecularcellular mechanisms related to NASH, cardiometabolic disease, and insulin resistance, including metabolic studies in obese diabetic mice. Priority will be given to candidates who have experience in these areas, particularly in conducting metabolic analyses in obese mice. The selected candidate will conduct research on the following projects: * NASH: We study the roles of different liver cell types in NASH development and progression, with current investigations focused on (a) the role of a transcription factor TAZ in both NASH fibrosis and NASH-associated hepatocellular carcinoma; (b) new mechanistic insight into human genetic risk factors for NASH fibrosis, with current focus on MERTK and PNPLA3; (c) mechanisms of efferocytosis in NASH; and (d) new therapeutic strategies to prevent steatosis-to-NASH progression based on our findings. * Advanced atherosclerosis: We have focused on integrated processes that promote advanced plaque progression, with the current focus on defective clearance of the apoptotic cells (efferocytosis) and impaired inflammation resolution. In the efferocytosis field, we study a process called continual efferocytosis, whereby a macrophage ingests and degrades multiple apoptotic cells over a short time period, requiring reprogramming of vesicular trafficking pathways and metabolism of molecules from degraded apoptotic cells. The inflammation resolution project investigates cellular mechanisms of the resolution process and its therapeutic potential, e.g., through the use of atherosclerosis-targeted nanoparticles packaged with resolution mediators. An exciting new area in the lab involves identifying specific mechanistic links between impaired resolution pathways and clonal hematopoiesis of indeterminate potential (CHIP), which is a major risk factor for atherosclerosis and coronary artery disease in humans over the age of 60. * Insulin resistance: The lab's studies on hepatic insulin resistance, which is an important driver of atherosclerosis, led to the discovery of a new calcium-stimulated pathway in hepatocytes that plays a key role in glucagon-mediated excessive glucose production, insulin resistance, fatty liver, dyslipidemia, impaired thrombolysis, and adipose tissue inflammation in the setting mechanisms involved in this new pathway; (b) how the pathway may promote atherosclerotic plaque progression by affecting plaque macrophages; and (c) strategies to translate our discoveries into new types of drugs to treat type 2 diabetes and prevent diabetes-driven atherosclerotic plaque progression.


Minimum Degree Required: Ph.D., MD or both

Minimum Qualifications: No more than 2.5 years post-graduation for PhD graduates; (2) first author high-quality publications published in first-rate journals; (3) experience in the research areas outlined above

Columbia University is an Equal Opportunity Employer / Disability / Veteran

Pay Transparency Disclosure

The salary of the finalist selected for this role will be set based on a variety of factors, including but not limited to departmental budgets, qualifications, experience, education, licenses, specialty, and training. The above hiring range represents the University's good faith and reasonable estimate of the range of possible compensation at the time of posting.

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