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|Start Date / Time||November 9, 2016 at 9:00 AM|
|End Date / Time||November 9, 2016 at 9:55 AM|
|Location||512 Light Hall|
|Presenter Name||Hannah Worchel (Magnuson lab)|
|Presentation Title||Pancreatic Inflammation Redirects Acinar to Beta Cell Reprogramming|
|Status||This meeting has already occurred|
Adenoviral delivery of Pdx1, Neurog3 and MafA (3TF) to the pancreas of mice has been shown to reprogram pancreatic acinar cells into insulin-expressing beta-like cells. However, for pancreatic cellular reprogramming to ever become a viable human therapy, a greater understanding of the factors that both promote and limit reprogramming as well as the affects that acinar to beta-cell conversion has on pancreas histology and physiology is required. Using a novel mouse model that expresses 3TF in both a pancreatic acinar cell- and doxycycline-dependent manner, we discovered that the outcome of transcription factor-mediated acinar to beta-cell reprogramming is highly dependent on both the magnitude of 3TF expression and reprogramming-induced inflammation.