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| Funder | Wellcome Trust |
|---|---|
| Recipient Organization | University of Edinburgh |
| Country | United Kingdom |
| Start Date | Aug 09, 2021 |
| End Date | Aug 08, 2024 |
| Duration | 1,095 days |
| Number of Grantees | 1 |
| Roles | Award Holder |
| Data Source | Europe PMC |
| Grant ID | 225470 |
Autophagy or ‘self-eating’ is a process by which cells remove unnecessary or dysfunctional cellular components by transporting them to the lysosome (the waste disposal system of the cell). My work is going to be focussed on autophagy of the endoplasmic reticulum (ER), known as ER-phagy. The endoplasmic reticulum is an organelle that is critical for protein synthesis.
The ER is particularly important in professional secretory cells such as the acinar cells of the pancreas (the cells that produce digestive enzymes).
Our lab previously discovered that a gene called Ccpg1 is important in ER-phagy and helps to protect the ER from stress and damage.
In mice, Ccpg1 is switched off in early pancreatic cancer lesions and decreased levels of Ccpg1 appear to increase the rate at which pancreatic cancer develops.
I plan to study the role of Ccpg1 and other genes involved in ER-phagy during the very early changes in the pancreatic acinar cells that can lead to pancreatic cancer. I will also try to find out how signals coming from these cells are altered during the formation of cancer. These investigations will help me to determine key genes and pathways involved in the formation of pancreatic cancer.
University of Edinburgh
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