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Ercument Dirice, Ph.D.

Ercument Dirice, Ph.D.Assistant Professor

Contact Information:



Department of Pharmacology
Basic Science Building, Rm. 21
15 Dana Road, Valhalla, NY 10595

Professional Interest

Despite the widespread belief that beta cells are completely lost in the latter stage of type 1 diabetes (T1D), this is not always true. Evidence shows that patients with long-term T1D (>50 years) exhibit persistent insulin-positive beta cells that are able to survive and even replicate.  The major thrust of the Dirice Lab is to elucidate the role of heterogeneity in beta cells and their vitality and dysfunction, particularly in diabetes. Of acute interest is the utilization of naturally occurring mechanisms regulating beta cell survival and their resistance to stress-mediated apoptosis. Certain beta cell subpopulations which uniquely facilitate specialized tasks to adapt or protect themselves during different physiologic and pathophysiologic conditions have the potential to be harnessed to develop novel therapeutic approaches that protect against beta cell loss; the characteristic phenomenon in both type 1 and type 2 diabetes (T2D). While recent studies have increased our understanding of β-cell heterogeneity, we need to further harness technological advances and smart study designs to characterize and exploit β-cell heterogeneity in therapies for T1D and T2D. Dr. Dirice has a long record of work in islet biology, especially in utilizing methods of research like transgenic mouse models, islet isolation and transplantation, and genetic analysis. His more recent research has contributed to the progression of understanding beta cell proliferation and survival through chemical and physiological means. In these works, he has reported the protection against diabetes from preemptive beta cell population growth, the anti-infiltration effect of HDAC3 on diabetic islets, and the role of DYRK1A in stimulation human beta cell reproduction.

Selected Bibliography

  1. Increased β-cell proliferation before immune cell invasion prevents progression of type 1 diabetes.
    Dirice E, Kahraman S, De Jesus DF, El Ouaamari A, Basile G, Baker RL, Yigit B, Piehowski PD, Kim MJ, Dwyer AJ, Ng RWS, Schuster C, Vethe H, Martinov T, Ishikawa Y, Teo AKK, Smith RD, Hu J, Haskins K, Serwold T, Qian WJ, Fife BT, Kissler S, Kulkarni RN.Nat Metab. 2019 May;1(5):509-518. doi: 10.1038/s42255-019-0061-8. Epub 2019 May 6.PMID: 31423480 Free PMC article.
  2. Inhibition of DYRK1A Stimulates Human β-Cell Proliferation.
    Dirice E, Walpita D, Vetere A, Meier BC, Kahraman S, Hu J, Dančík V, Burns SM, Gilbert TJ, Olson DE, Clemons PA, Kulkarni RN, Wagner BK.Diabetes. 2016 Jun;65(6):1660-71. doi: 10.2337/db15-1127. Epub 2016 Mar 7.PMID: 26953159 Free PMC article.
  3. Soluble factors secreted by T cells promote β-cell proliferation.
    Dirice E, Kahraman S, Jiang W, El Ouaamari A, De Jesus DF, Teo AK, Hu J, Kawamori D, Gaglia JL, Mathis D, Kulkarni RN.Diabetes. 2014 Jan;63(1):188-202. doi: 10.2337/db13-0204. Epub 2013 Oct 2.PMID: 24089508 Free PMC article.
  4. Isoform-selective inhibitor of histone deacetylase 3 (HDAC3) limits pancreatic islet infiltration and protects female nonobese diabetic mice from diabetes.
    Dirice E, Ng RWS, Martinez R, Hu J, Wagner FF, Holson EB, Wagner BK, Kulkarni RN.J Biol Chem. 2017 Oct 27;292(43):17598-17608. doi: 10.1074/jbc.M117.804328. Epub 2017 Aug 31.PMID: 28860191 Free PMC article.
  5. Inhibition of TGF-β Signaling Promotes Human Pancreatic β-Cell Replication.
    Dhawan S, Dirice E, Kulkarni RN, Bhushan A.Diabetes. 2016 May;65(5):1208-18. doi: 10.2337/db15-1331. Epub 2016 Mar 2.PMID: 26936960 Free PMC article.