In response to RFA-DK-09-504 we present a plan for future activities of the Coordinating Center for the Beta Cell Biology Consortium (BCBC). This consortium, which was initially launched in September 2001 then renewed in 2005, brings a team-oriented approach to studies necessary to learn how to regenerate or replace pancreatic beta cells that are either destroyed or damaged by Type 1 or Type 2 diabetes. The Coordinating Center plays a vital role in the consortium by 1) organizing investigator meetings and retreats, 2) maintaining the BCBC website and reagent databases, 3) overseeing BCBC core facilities, 4) providing advanced bio/informatics applications, 5) managing special funding programs, 6) providing various types of administrative support, and 7) facilitating interactions with other NIH-sponsored Centers and Consortia. During the next cycle of the BCBC the Coordinating Center will 1) continue to perform many ongoing operations, 2) adapt to changes in the scientific focus and new participants, and 3) improve the website in a way to facilitate team science and sharing of unpublished knowledge and reagents.

Public Health Relevance

Type 1 and Type 2 diabetes cause significant morbidity and mortality and thus have an adverse economic impact. Both diseases are characterized by the destruction or dysfunction of insulin-secreting pancreatic beta cells. This application will coordinate activities among a team of scientists in order to develop new, cell-based replacement therapies that hold promise for achieving better glucose control than is currently possible.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Research Project--Cooperative Agreements (U01)
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Special Emphasis Panel (ZDK1-GRB-G (M3))
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Sato, Sheryl M
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Vanderbilt University Medical Center
Schools of Medicine
United States
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Dai, Chunhua; Hang, Yan; Shostak, Alena et al. (2017) Age-dependent human ? cell proliferation induced by glucagon-like peptide 1 and calcineurin signaling. J Clin Invest 127:3835-3844
Westacott, Matthew J; Farnsworth, Nikki L; St Clair, Joshua R et al. (2017) Age-Dependent Decline in the Coordinated [Ca2+] and Insulin Secretory Dynamics in Human Pancreatic Islets. Diabetes 66:2436-2445
Spaeth, Jason M; Gupte, Manisha; Perelis, Mark et al. (2017) Defining a Novel Role for the Pdx1 Transcription Factor in Islet ?-Cell Maturation and Proliferation During Weaning. Diabetes 66:2830-2839
Bechard, Matthew E; Bankaitis, Eric D; Ustione, Alessandro et al. (2017) FUCCI tracking shows cell-cycle-dependent Neurog3 variation in pancreatic progenitors. Genesis 55:
Olehnik, Scott K; Fowler, Jonas L; Avramovich, Gil et al. (2017) Quantitative analysis of intra- and inter-individual variability of human beta-cell mass. Sci Rep 7:16398
Aamodt, Kristie I; Powers, Alvin C (2017) Signals in the pancreatic islet microenvironment influence ?-cell proliferation. Diabetes Obes Metab 19 Suppl 1:124-136
Stancill, Jennifer S; Cartailler, Jean-Philippe; Clayton, Hannah W et al. (2017) Chronic ?-Cell Depolarization Impairs ?-Cell Identity by Disrupting a Network of Ca2+-Regulated Genes. Diabetes 66:2175-2187
Cogger, Kathryn F; Sinha, Ankit; Sarangi, Farida et al. (2017) Glycoprotein 2 is a specific cell surface marker of human pancreatic progenitors. Nat Commun 8:331
Dean, E Danielle; Li, Mingyu; Prasad, Nripesh et al. (2017) Interrupted Glucagon Signaling Reveals Hepatic ? Cell Axis and Role for L-Glutamine in ? Cell Proliferation. Cell Metab 25:1362-1373.e5
Yang, Yu-Ping; Magnuson, Mark A; Stein, Roland et al. (2017) The mammal-specific Pdx1 Area II enhancer has multiple essential functions in early endocrine cell specification and postnatal ?-cell maturation. Development 144:248-257

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