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Publication

Mice deficient in GEM GTPase show abnormal glucose homeostasis due to defects in beta-cell calcium handling.

Jenny E Gunton | Mary Sisavanh | Rebecca A Stokes | Jon Satin | Leslie S Satin | Min Zhang | Sue M Liu | Weikang Cai | Kim Cheng | Gregory J Cooney | D Ross Laybutt | Trina So | Juan-Carlos Molero | Shane T Grey | Douglas A Andres | Michael S Rolph | Charles R Mackay
PloS one | 2012

Glucose-stimulated insulin secretion from beta-cells is a tightly regulated process that requires calcium flux to trigger exocytosis of insulin-containing vesicles. Regulation of calcium handling in beta-cells remains incompletely understood. Gem, a member of the RGK (Rad/Gem/Kir) family regulates calcium channel handling in other cell types, and Gem over-expression inhibits insulin release in insulin-secreting Min6 cells. The aim of this study was to explore the role of Gem in insulin secretion. We hypothesised that Gem may regulate insulin secretion and thus affect glucose tolerance in vivo.

Pubmed ID: 22761801

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Associated grants

  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK46409
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK046409
  • Agency: NHLBI NIH HHS, United States
    Id: R01 HL074091
  • Agency: Medical Research Council, United Kingdom
  • Agency: NHLBI NIH HHS, United States
    Id: R01 HL072936
  • Agency: NIDDK NIH HHS, United States
    Id: P30 DK020572

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C57BL/6J (tool)

RRID:IMSR_JAX:000664

Mus musculus with name C57BL/6J from IMSR.

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