Pharmacological inhibition of Eph receptors enhances glucose-stimulated insulin 
secretion from mouse and human pancreatic islets.

Jain, Ruchi; Jain, D; Liu, Q; Bartosinska, B; Wang, J; Schumann, D; Kauschke, S G; Eickelmann, Peter; Piemonti, Lorenzo; Gray, N S; Lammert, Eckhard

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Pharmacological inhibition of Eph receptors enhances glucose-stimulated insulin secretion from mouse and human pancreatic islets.

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Jain, Ruchi
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Lammert, Eckhard
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Citation

Jain, R., Jain, D., Liu, Q., Bartosinska, B., Wang, J., Schumann, D., et al. (2013). Pharmacological inhibition of Eph receptors enhances glucose-stimulated insulin secretion from mouse and human pancreatic islets. Diabetologia, 56(6), 1350-1355.

Cite as: http://hdl.handle.net/21.11116/0000-0001-0720-3

Abstract

Type 2 diabetes is characterised by impaired glucose-stimulated insulin secretion (GSIS) from pancreatic islets. Since erythropoietin-producing hepatoma (Eph)-ephrin bidirectional signalling fine-tunes GSIS from pancreatic beta cells, we investigated Eph receptor tyrosine kinases (RTK) as potential drug targets for selectively increasing GSIS.