Supplementary Materials

The PDF file includes:

  • Materials and Methods
  • Fig. S1. Combination of DYRK1A inhibitors with GLP1R agonists yields synergistic increases in human β cell proliferation.
  • Fig. S2. The DYRK1A–GLP-1 increase human β cell numbers is a class effect for both DYRK1A inhibitors and GLP1R agonists.
  • Fig. S3. The effects of the harmine–GLP-1 combination on proliferation in non–β cells, β cell death, and DNA damage.
  • Fig. S4. Evaluation of the role of DYRK1A and cAMP signaling in harmine–GLP1R agonist synergy.
  • Fig. S5. GLP1R signaling diagram.
  • Fig. S6. Additional evaluation of the role cAMP pathway signaling in harmine–GLP1R agonist synergy.
  • Fig. S7. Mechanisms downstream of the GLP1R.
  • Fig. S8. Harmine–GLP-1 treatment maintains or enhances human β cell differentiation.
  • Fig. S9. A magnified confocal view of GLUT2 trafficking.
  • Fig. S10. Glucose-stimulated insulin secretion from normal and T2D islets.
  • Fig. S11. Effects of harmine–GLP-1 on β cells from individuals with T2D.
  • Fig. S12. Effects of the harmine–exendin-4 combination on human β cells in immunodeficient mice.
  • Fig. S13. Blood glucose values in euglycemic mice treated with saline, exendin-4, harmine, or their combination.
  • Fig. S14. Effects of the harmine–exendin-4 combination on normal organ histopathology and ductal proliferation in NSG mice.

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Human islet donor demographic data.
  • Data file S2 (Microsoft Excel format). Primary and secondary antisera.
  • Data file S3 (Microsoft Excel format). qPCR primers.