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Biography

Anath Shalev joined the faculty of the University of Wisconsin in 2002 as an Assistant Professor of Medicine. She graduated from the University of Basel, Switzerland and completed a post-graduate Scholarship in Experimental Medicine and Biology at the University of Zurich and a Research Fellowship at Harvard. For her fellowship in Endocrinology, Diabetes and Metabolism Dr. Shalev went to the National Institutes of Health and after completing her training continued to serve as an Endocrine Consult Attending and Senior NIDDK Research Fellow prior to coming to Madison. Currently, Dr. Shalev is a tenured Associate Professor of Medicine and Pharmacology and serves as the Research Director of the Endocrinology, Diabetes and Metabolism Section. She also is an active trainer in the Cellular and Molecular Biology (CMB) and Endocrine & Reproductive Physiology (ERP) Programs and a member of the UW Comprehensive Cancer Center (UWCCC).

Dr. Shalev maintains an active clinical Endocrinology practice with interests including thyroid cancer/disorders, multiple endocrine neoplasias (MEN) and diabetes.

In addition to teaching and mentoring graduate students, post-docs and MDs, Dr. Shalev's main interests include her laboratory, which focuses on molecular diabetes and cancer research, mechanisms of apoptosis and regulation of gene transcription.

Research Focus

Diabetes is a rapidly growing public health issue characterized by elevated blood glucose levels and high morbidity and mortality. Under normal conditions, insulin, a hormone produced exclusively in the pancreatic beta cells, maintains blood glucose levels within the normal range. Loss of these pancreatic beta cells by programmed cell death (apoptosis) is a key feature of diabetes. Therefore, finding a target that could be used to block beta cell apoptosis and thereby preserve the patient's own beta cell mass and insulin production would represent a major breakthrough for diabetes therapy. However, the mechanisms involved in beta cell death are not well understood. The Shalev laboratory recently identified thioredoxin-interacting protein (TXNIP) (a protein involved in the cellular redox state) as such a potential target. When performing the first human pancreatic islet microarray study, Shalev found that TXNIP was the most dramatically up-regulated gene in response to glucose, suggesting that it might play an important role in beta cell biology. Subsequent analysis of the TXNIP promoter revealed that a unique carbohydrate response element was responsible for this glucose-induced TXNIP transcription. The Shalev group went on to show that TXNIP expression is increased in islets of mice with diabetes and that TXNIP overexpression induces beta cell apoptosis. Moreover, the Shalev lab found that TXNIP plays a critical role in linking glucose toxicity to beta cell death and that TXNIP deficiency promotes beta cell survival and prevents diabetes. Still, very little is known about the processes controlling TXNIP and the Shalev lab is therefore now employing molecular biological in vitro approaches, as well as cell culture and various in vivo mouse models, to study the molecular mechanisms and signaling pathways involved in TXNIP regulation and function. Additional ongoing projects include the study of the role of TXNIP in diabetic heart failure as well as in cancer.

Search for Anath Shalev's literature abstracts on PubMed

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