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Ira Tabas

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Ira Tabas is an American molecular biologist who currently serves as Richard J. Stock Professor and Vice-Chair of Research in the Department of Medicine, Professor of Anatomy & Cell Biology at Columbia University in the City of New York, and an endocrinologist affiliated with NewYork–Presbyterian Hospital .[1]

Biography

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Tabas attended Washington University in St. Louis, Missouri, where he received his medical degree and his doctorate in biochemistry. While completing an internship and residency in internal medicine and a fellowship in endocrinology and metabolism at Columbia University Medical Center in New York City, he also conducted a postdoctoral fellowship in Alan Tall laboratory in the Department of Medicine at Columbia University. He began his independent scientific career as a Columbia faculty in 1985, and currently serves as Vice-Chair of Research in the Department of Medicine [2]

Research contributions

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Cellular biology of advanced atherosclerotic plaque progression

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A major research focus of Tabas is the molecular and cellular mechanisms and consequences resulting from macrophage apoptosis and from phagocytic clearance of apoptotic cells in advanced atherosclerotic lesions. One notable finding showed a critical link between the PERK / CHOP branch of the stress Unfolded protein response (UPR) and a calcium-induced apoptosis pathway, which involves an ER calcium-release channel IP3R, a calcium-sensitive protein kinase called CaMKII, and an oxidative stress-generating enzyme NADPH[3][4][5][6]

Tabas developed nanoparticles that encapsulate and release an inflammation-resolving peptide drug. These nanomedicines can selectively home to tissue injury sites in mice, and release in a controlled manner over time.[7][8]

Molecular mechanism linking insulin resistance to enhanced atherosclerosis

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Tabas discovered a calcium-IP3R-CaMKII pathway plays a key role in glucagon-mediated excessive hepatic glucose production, insulin resistance, fatty liver, and dyslipidemia in the setting of obesity and type 2 diabetes.[9][10][11][12][13]

Awards and honors

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  • 1988 American Heart Association Established Investigator Award[14]
  • 1990 Columbia University Doctor Harold and Golden Lamport Research Award[citation needed]
  • 2000 Richard J. Stock Professorship in the Department of Medicine of Columbia University[citation needed]
  • 2011 Elected to Board of Reviewing Editors for Science[15]
  • 2014 Bonazinga award: "Presented annually to a Society of Leukocyte Biology member for excellence in leukocyte biology research. It is the highest honor the society can bestow upon one of its members and has been awarded annually since 1980."[citation needed]

References

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  1. ^ Tabas, Ira. "Professor of Medicine and Pathology & Cell Biology". Columbia University. Retrieved May 5, 2016.
  2. ^ Tabas, Ira. "Biography". NYP. Retrieved May 17, 2016.
  3. ^ "What separates dangerous blood vessel plaques from benign ones". (e) Science News. May 5, 2009. Retrieved May 18, 2016.
  4. ^ Thorp, E; Li, G; Seimon, TA; Kuriakose, G; Ron, D; Tabas, I (2009). "Thorp, E., Li, G., Seimon, T. A., Kuriakose G., Ron D., Tabas, I.A. (2009) Reduced apoptosis and plaque necrosis in advanced atherosclerotic lesions of Apoe-/- and Ldlr-/- mice lacking CHOP". Cell Metabolism. 9 (5): 474–81. doi:10.1016/j.cmet.2009.03.003. PMC 2695925. PMID 19416717.
  5. ^ Tabas, I (2009). "Tabas, I. (2009) Macrophage death and defective inflammation resolution in atherosclerosis". Nature Reviews Immunology. 10 (1): 36–46. doi:10.1038/nri2675. PMC 2854623. PMID 19960040.
  6. ^ Tabas, I (2010). "Tabas, I., (2010) The role of endoplasmic reticulum stress in the progression of atherosclerosis". Circulation Research. 107 (7): 839–50. doi:10.1161/CIRCRESAHA.110.224766. PMC 2951143. PMID 20884885.
  7. ^ "Keeping atherosclerosis in-check with novel targeted inflammation-resolving nanomedicines". Science Daily. February 18, 2015. Retrieved May 18, 2016.
  8. ^ "Scientists develop a biodegradable nanoparticle that effectively resolves inflammation". Phys.org. March 18, 2013. Retrieved May 18, 2016.
  9. ^ Fiore, Kristina (November 24, 2013). "Mouse Studies Point to Kinase as Diabetes Treatment Target". MedPageToday. Retrieved May 18, 2016.
  10. ^ "Targeting glucagon pathway may offer a new approach to treating diabetes". Science Daily. April 12, 2012. Retrieved May 18, 2016.
  11. ^ "Prolonged stress sparks ER to release calcium stores and induce cell death in aging-related diseases". (e) news engine. September 14, 2009. Retrieved May 18, 2016.
  12. ^ Ozcan, L; Wong, CC; Li, G; Xu, T; Pajvani, U; Park, SK; Wronska, A; Chen, BX; Marks, AR; Fukamizu, A; Backs, J; Singer, HA; Yates, JR; Accili, D; Tabas, I (2012). "Lale Ozcan, Catherine C.L. Wong, Gang Li,1 Tao Xu, Utpal Pajvani, Sung Kyu Robin Park, Anetta Wronska, Bi-Xing Chen, Andrew R. Marks, Akiyoshi Fukamizu, Johannes Backs, Harold A. Singer, John R. Yates, III, Domenico Accili, and Ira Tabas (2012). Calcium signaling through CaMKII regulates hepatic glucose production in fasting and obesity". Cell Metabolism. 15 (5): 739–51. doi:10.1016/j.cmet.2012.03.002. PMC 3348356. PMID 22503562.
  13. ^ Ozcan, L; Cristina; de Souza, J; Harari, AA; Backs, J; Olson, EN; Tabas, I (2013). "Lale Ozcan, Jane Cristina de Souza, Alp Avi Harari, Johannes Backs, Eric N. Olson, and Ira Tabas (2013). Activation of calcium/calmodulin-dependent protein kinase II in obesity mediates suppression of hepatic insulin signaling". Cell Metabolism. 18 (6): 803–15. doi:10.1016/j.cmet.2013.10.011. PMC 3863383. PMID 24268736.
  14. ^ Tabas, Ira. "Ira Tabas CV" (PDF). Tabaslab.com. Retrieved May 17, 2016.
  15. ^ "Science Editors and Editorial Boards". Sciencemag.org. Retrieved May 18, 2016.
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