Grant Funding
Active Grants:
2006-2017 R01 DK074656
Title: mt-Nd2 and Resistance to Autoimmune Diabetes
Project Role: Principal Investigator (40% Effort)
Source: National Institutes of Health (NIDDK/NIAID)
Total Award: $1,665,000 ($225,000/ year Direct)
Objective: Understand the role that the C278A sequence variation in mt-Nd2 plays in resistance to T1D.
2010-2013 JDRF 25-2010-688
Title: Islet Resistance to T1D (nPOD)
Project Role: Principal Investigator (5% Effort)
Source: Juvenile Diabetes Foundation International
Total Award: $110,000 ($50,000/ year Direct)
Objective: Determine metabolic differences in the pancreatic islets comparing organs from individuals with T1D and those that have circulating autoantibodies to b cell antigens but do not have T1D.
2011-2014 ADA 1-11-BS-104
Title: Idd22 controls resistance to autoimmune diabetes at the beta cell level
Project Role: Principal Investigator (10% Effort)
Source: American Diabetes Assocition (ADA)
Total Award: $313,500 ($95,000/ year Direct)
Objective: Identify Idd22 and the mechanism of b cell resistance.
2013-2015 JDRF 17-2012-595
Title: Lymphocyte Mitochondrial Dysfunction in Type 1 Diabetes
Project Role: Co-Principal Investigator (10% Effort)
Source: Juvenile Diabetes Research Foundation (JDRF)
Total Award: $495,000 ($150,000/ year Direct)
Objective: Identify and determine novel lymphocyte mitochondrial biomarkers associated with Type 1 Diabetes
PENDING Support
R01AI103226-A1 9/1/2013-8/31/2018
Source: National Institutes of Health (NIDDK)
Title: Divergent control of autoimmunity in T1D and SLE through the G-CSF pathway
Project Role: Co-Investigator
Objective: This application will test the hypothesis that the G-CSF signaling pathway is critical to the pathogenesis of T1D and SLE and modulation of this pathway in opposite directions for the two autoimmune diseases will lead to disease prevention.
P01AI42288 (Atkinson, P.I.) Competitive Renewal 9/01/13 – 08/31/18
Source: National Institutes of Health NIAID
Title: Immune Function and the Progression to Type I Diabetes
Role: Co-Principal Investigator Project 2
Objective: To test our overall hypothesis that T1D results from a combination of genetic variants that negatively impact regulatory mechanisms, leading to a tissue-specific break in tolerance and islet b cell dysfunction and death
AN:3525662 9/01/13 – 08/31/18
Source: National Institutes of Health NIAID
Title: Interferon a/b in Type 1 Diabetes Pathogenesis
Role: Principal Investigator (Multi-PI With Michael Clare-Salzler)
Objective: To define the IFN roles in regulating both acquired and innate responses associated with the pathology and immunogenetics of Type 1 Diabetes
Completed Support
2007-2010 JDRF 1-2007-77
Title: Identification of Susp and the role of Susp in T1D-Resistance
Project Role: Principal Investigator (20% Effort)
Source: Juvenile Diabetes Foundation International
Total Award: $462,000 ($140,000/ year Direct)
Objective: Define the T1D protective gene that is Susp, and examine the role of Susp in protection against T1D.
2003-2008 U19 AI056374
Title: Utilization of ALR Derived T1D Resistance Loci to Improve Islet Graft Outcome
Project Role: Principal Investigator
Source: National Institutes of Health (NIAID)
Total Award: $1,480,000
Objective: to determine if the heritable resistance of ALR islets to autoimmunity will extend to a defense against both allo-graft and auto-graft rejection
2000-2007 ERMS# 00035010 (PI: Massimo Trucco)
Title: New Advanced Technology to Improve Prediction and Prevention of Type 1 Diabetes
Project Role: Co-Investigator
Source: Department of Defense
Total Award: $4,936,454 ($715,786/ year Direct)
Objective: To utilize new technology, increasing the speed and relieving economic strain of genetic screening in large populations studies.
2007-2008 Smith and Nephew Diabetes Project (PI: Jeffrey Hollinger, Carnegie Mellon University)
Title: Bone Wound Healing in the Akita model of type 1 Diabetes
Project Role: Subcontract to Clayton E. Mathews
Source: Smith & Nephew Inc.
Direct Cost of Subcontract: $50,000 Annual
Objective: Determine whether “bioactive molecule 1” and “bioactive molecule 2” enhance bone wound healing in the C57BL/6-Ins2Akita model of insulin requiring diabetes.
2006-2007 JDFI 5-2006-232
Title: Generation of Cybrids to Study a mtDNA SNP Associated with T1D
Project Role: Principal Investigator
Source: Juvenile Diabetes Foundation International
Total Award: $108,900 ($100,000/ year Direct)
Objective: To generate and study cell lines with a polymorphism in the mitochondrial DNA polymorphism that is protective against Type 1 Diabetes.
2001-2006 JDFI 2-2001-860
Title: Genetics of Resistance to Immune-Mediated Beta Cell Destruction
Project Role: Principal Investigator
Source: Juvenile Diabetes Foundation International
Total Award: $693,750 ($125,000/ year Direct)
Objective: Fine map Insulin Dependant Diabetes resistance loci and elucidate the molecular basis for the unique resistance of ALR to immune-mediated injury
NOTE: This grant was submitted for renewal July 14th, 2006. Listed as #2 under the Pending Support Section.
1999-2001 NIH F32 DK09865
Title: Mechanisms of susceptibility to alloxan in mice
Project Role: Principal Investigator
Source: National Institutes of Health (NIDDK)
Total Award: $201,600 ($40,000/ year Direct)
Objective: Establish the genetic and biochemical basis for the differential susceptibility of ALR and ALS strains to chemically-induced diabetes.
1999-2002 ADA EHL, Inc.
Title: Molecular genetics of free radical defenses in alloxan resistant (ALR) mice
Project Role: Co-Principal Investigator
Source: American Diabetes Association
Total Award: $333,000 ($100,000/ year Direct)
Objective: Identify both the genetic map location and the function of the gene or genes conferring upon ALR/Lt mice such remarkable resistance to ROS damage.
1999-2001 JDF 1-1999-642
Title: Genetic up-regulation of free radical defenses to prevent IDDM in NOD mice
Project Role: Co-Principal Investigator
Source: Juvenile Diabetes Foundation International
Total Award: $222,000 ($100,000/ year Direct)
Objective: Examine the resistance of ALR islets to autoimmune effector mediated stress.