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| Funder | Diabetes UK |
|---|---|
| Recipient Organization | University of Birmingham |
| Country | United Kingdom |
| Start Date | Mar 01, 2021 |
| End Date | Aug 30, 2025 |
| Duration | 1,643 days |
| Number of Grantees | 1 |
| Roles | Award Holder |
| Data Source | Europe PMC |
| Grant ID | 20/0006136 |
Diabetes is a chronic condition that occurs when the pancreatic beta-cells are destroyed or cannot secrete enough of the hormone insulin to keep up with the demand.
Cell replacement therapies aim to generate insulin-producing beta-like cells from stem cells in order to replace or aid the failing innate beta-cells of people living with diabetes. This therapy has great potential and has recently advanced to clinical trials.
However, beta-like cells generated from stem cells cannot perform glucose stimulated insulin secretion (GSIS) in the same capacity as innate beta-cells. This impedes their use in broader clinical applications.
This proposal aims to identify and characterize key regulators of GSIS and other insulin-related pathways in the beta-cell in order to improve beta-cell generation protocols from stem cells.
Transcription factors are key regulators of cellular identity and are responsible for orchestrating both specific and ubiquitous functions in a cell.
Using computational analysis, we identified previously unknown candidate transcription factors that likely control GSIS in the pancreatic beta-cells.
We aim to characterize their impact on the beta-cell function and use this knowledge to improve the functionality of stem cell generated beta-cells, with particular emphasis on GSIS.
University of Birmingham
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