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Grant: Operating Grant - Priority Announcement: INMD Start Up Funds (bridge funding)

University of British Columbia

$100,000.00

Functional analysis of Myt3's role in Beta-cell transcriptional networks and diabetes

FY 2009-10

Summary
Type 1 Diabetes, an autoimmune disease caused by a patients immune cells killing the body's insulin producing Beta-cells, is a major health concern in Canada. Transplantation of donor islets can cure Type 1 diabetic patients; however, the transplanted cells often fail due to attack by the recipient's immune cells. Immune cells secret compounds called cytokines that induce Beta-cell death, or apoptosis. A great deal remains unknown about how apoptosis occurs within Beta-cells and how it is controlled. Understanding these processes is essential for developing novel strategies to cure Type 1 Diabetes. What is known is that exposure to immune cell produced cytokines changes the expression of many genes within Beta-cells; in fact this turns on the expression of several genes involved in apoptosis. How these genes are turned on, and how they are normally kept off, are not understood. Transcription factors are proteins that control gene expression, and we have identified a transcription factor called Myt3 that is almost exclusively expressed in islet cell types and whose expression is significantly reduced by Beta-cell exposure to cytokines. We believe that Myt3 normally prevents the expression of genes that induce apoptosis. By manipulating it's expression we hypothesize we will reduce Beta-cell apoptosis in response to cytokine exposure. We believe that this will bring us one step closer to a cure for Type 1 Diabetes.
Program
Operating Grant - Priority Announcement: INMD Start Up Funds (bridge funding)
Location
British Columbia, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
198290
Name
Hoffman Brad G
Region
British Columbia
Country
Canada
Orgtype
Research Institution; Institution Paid
Instname2
Nutrition, Metabolism and Diabetes
Theme2
Biomedical
Prcname2
Diabetes, Obesity, Lipid & Lipoprotein Disorders
Projecttitle
Functional analysis of Myt3's role in Beta-cell transcriptional networks and diabetes
Programtype2
Operating Grants
Orgnameinp2
University of British Columbia
Cihramount2
$100,000
Cihrequipment2
$0
Programname2
Operating Grant - Priority Announcement: INMD Start Up Funds (bridge funding)
Keyworddelim
Apoptosis; Diabetes; Gene Regulation; Proliferation; Transcription Factors
Abstract
Type 1 Diabetes, an autoimmune disease caused by a patients immune cells killing the body's insulin producing Beta-cells, is a major health concern in Canada. Transplantation of donor islets can cure Type 1 diabetic patients; however, the transplanted cells often fail due to attack by the recipient's immune cells. Immune cells secret compounds called cytokines that induce Beta-cell death, or apoptosis. A great deal remains unknown about how apoptosis occurs within Beta-cells and how it is controlled. Understanding these processes is essential for developing novel strategies to cure Type 1 Diabetes. What is known is that exposure to immune cell produced cytokines changes the expression of many genes within Beta-cells; in fact this turns on the expression of several genes involved in apoptosis. How these genes are turned on, and how they are normally kept off, are not understood. Transcription factors are proteins that control gene expression, and we have identified a transcription factor called Myt3 that is almost exclusively expressed in islet cell types and whose expression is significantly reduced by Beta-cell exposure to cytokines. We believe that Myt3 normally prevents the expression of genes that induce apoptosis. By manipulating it's expression we hypothesize we will reduce Beta-cell apoptosis in response to cytokine exposure. We believe that this will bring us one step closer to a cure for Type 1 Diabetes.
Competitiondate
200909
Approvedterm2
1 yr 0 mth
Pinamesdelim
Hoffman, Brad G
Approvedterm
1 an 0 mois
Cihrcontribution2
~ $100,000~ $0~