Research in the Sander group is focused on understanding the molecular mechanisms that underlie the formation and function of insulin-producing beta cells in the pancreas, which are affected in diabetes. Our laboratory aims to identify strategies for beta cell regeneration and replacement in order to develop novel treatments for diabetes.

To understand cellular processes leading to diabetes, we employ genetic human pluripotent stem cell (hPSC)-based and mouse models. We interrogate these models with massively parallel sequencing and bioinformatic approaches and use functional assays to link molecular phenotypes to cell function and whole body physiology.

Our research is multi-disciplinary and highly collaborative. As part of the NIH-funded Human Islet Research Network (HIRN) we are generating a 3D islet organoid on a Chip and as part of the NIH-funded T2D-GENES Consortium we are using hPSC models to establish how genetic risk for diabetes causes cellular phenotypes.

We are looking for a postdoctoral researcher/senior scientist for integrative analysis of single cell data.

Congratulations to Wen and Nick on their new jobs!

Dr. Maike Sander receives the Humboldt Research Award

@msanderlab

- July 17, 2019

Insulin-reporter imaging shows transition between insulin-hi/low states in beta cells. Mechanisms/kinetics still un… https://t.co/NkYEpPsyVk
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@msanderlab

- July 17, 2019

Co-culture of human pancreatic islets and ductal cells in a microfluidic device suggests that ductal cells influenc… https://t.co/VibkqgQRYQ
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@msanderlab

- July 12, 2019

Tremendously enjoyed Rene Maehr’s (@MaehrLab) visit to Sanford Consortium (@wicollabor8) and UCSD. Rene shared his… https://t.co/ZLtX4bJolF
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@msanderlab

- July 11, 2019

Check out our collaborative work with @kjgaulton and @CEpigenomics. In addition to cell type/state resolved maps of… https://t.co/zQSiwoKGuH
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@msanderlab

- June 23, 2019

RT @guy_rutter: Excited to see our report appear in Nat Metab demonstrating functional beta cell hierarchy in living mice and fish! https:/…
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