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| Funder | Diabetes UK |
|---|---|
| Recipient Organization | Early-Career Small Grant |
| Country | United Kingdom |
| Start Date | Mar 03, 2025 |
| End Date | Mar 02, 2026 |
| Duration | 364 days |
| Number of Grantees | 1 |
| Roles | Award Holder |
| Data Source | Europe PMC |
| Grant ID | 24/0006780 |
Cilia are antenna-like projections on the surface of cells that play a central role in transducing and regulating several signalling pathways.
Islet cells have cilia, and recent studies suggest that cilia are involved in glucose-stimulated-calcium-influx and insulin release from β-cells. Loss of cilia in β-cells is associated with impaired β-cell function and insulin secretion.
Interestingly, cilia dysfunction has been linked to an increased prevalence of autoimmune disorders, including type 1 diabetes (T1D). It is well established that cytotoxic T-cells attack β-cells, leading to their destruction and onset of T1D.
Cilia may play a role in this process, as they are involved in sensing environmental cues and have been shown to interact with immune cells.
As a preliminary step, I have performed an in-silico analysis of publicly available RNA-sequencing datasets of mouse and human islets in naïve and T1D state, and aligned the data with known cilia gene dataset.
My results indicate 25 cilia genes are downregulated in non-obese diabetic mice and 19 genes are downregulated in human T1D patients with 7 of these genes being common in both mice and human. Here, I outline a proposal to unravel the role of β-cell-specific cilia in the development and onset of T1D.
Early-Career Small Grant
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