Investigating the molecular mechanisms of beta-cell expansion factor a-induced beta-cell proliferation
Active Project Grant Awarded Last action
- Award ID
- F31DK141197
- Recipient
-
University Of Oregon UEI Z3FGN9MF92U2
- Awarding agency
-
National Institute of Diabetes and Digestive and Kidney Diseases
National Institutes of Health, Department of Health and Human Services
- Obligated
- $245,686
Award facts
- Assistance listing
- 93.847 Diabetes, Digestive, and Kidney Diseases Extramural Research
- Completion date 53% complete
- Place of performance
- Eugene, OR 97403, USA
Award details come from USAspending.gov.
Description
- Abstract
- Beta-cell expansion factor a (befa) is a secreted bacterial protein that induces the proliferation of β-cells and promotes proper endocrine function during early development in both zebrafish and mice. The molecular mechanisms by which befa induces β-cell proliferation and metabolic maturation are not known. Befa contains a structurally conserved sylf domain that mediates interactions with phospholipids and disrupts membrane integrity. The broad and long-term objective of this project is to learn the molecular mechanisms by which befa impacts pancreatic β-cells. This work has wide-reaching possibilities for the development of therapeutic interventions for both type i and type II diabetes through a better understanding of β-cell proliferation and metabolic maturation to aid in the production of human induced pluripotent stem cell-derived β-cells. The focus of this proposal is to investigate how befa's demonstrated membrane perturbing activity promotes β-cell proliferation and metabolic maturation. In specific aim 1, i will utilize single-cell resolution live imaging, genetic manipulation of zebrafish, and human induced pluripotent stem cells to investigate whether befa- induced intracellular calcium signaling promotes β-cell proliferation. In specific aim 2, i will utilize imaging of β-cell mitochondria membrane potential and morphology and human induced pluripotent stem cell derived β- cells to test whether befa's impacts on mitochondria promote β-cells' metabolic maturation. If successful, the outcome of this proposal will be a new understanding of how membrane perturbation in vivo can promote proliferation, insulin secretion, and metabolic maturation of the essential insulin-producing β-cells. I aim to translate my mechanistic findings to advance the in vitro production of functional β-cells for cell therapies of type i and type II diabetes. Furthermore, the molecular insights i will discover, research protocols i will develop, and skills i will acquire through these studies will promote my development as an independent scientist, β-cell biologist, and prepare me for my future career in understanding the molecular mechanisms of microbiome impacts on host health.
Transactions
| Action | Obligated | Date |
|---|---|---|
| Amendment | $49,538 | |
| Amendment | $564 | |
| Amendment | $564 | |
| Amendment | $48,755 | |
| Amendment | $0 | |
| Amendment | $48,755 | |
| Amendment | $48,755 | |
| Amendment | $0 | |
| Original award | $48,755 |
Quick answers
Who received award F31DK141197?
F31DK141197 was awarded to University Of Oregon by National Institute of Diabetes and Digestive and Kidney Diseases (National Institutes of Health) on June 23, 2025.
How much is award F31DK141197 worth?
$245,686 has been obligated on F31DK141197.
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