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Transgenic Mice Expressing CNO-sensitive Gq- or Gs-coupled Designer Receptors Selectively in Pancreatic Beta Cells
Case ID:
TAB-3042
Web Published:
12/6/2022
Description:
Impaired functioning of pancreatic beta cells is a key hallmark of type 2 diabetes. Beta cell function is modulated by the actions of different classes of heterotrimeric G proteins. The functional consequences of activating specific beta cell G protein signaling pathways in vivo are not well understood at present, primarily due to the fact that beta cell G protein-coupled receptors (GPCRs) are also expressed by many other tissues. To circumvent these difficulties, we developed a strategy that allows for the conditional and selective activation of specific beta cell G proteins in intact animals. Specifically, we created two lines of transgenic mice each of which expressed a specific designer GPCR (DREADD = Designer Receptor Exclusively Activated by a Designer Drug) in beta cells only (beta-RASSL-1 = RIPII-Rq Tg = beta Gq DREADD transgenic mice; beta-RASSL-2 = RIPII-Rs = beta Gs DREADD transgenic mice). Importantly, the two designer receptors differ in their G protein-coupling properties (Gq versus Gs). They are unable to bind endogenous ligand(s), but can be efficiently activated by an otherwise pharmacologically inert compound (clozapine-N-oxide = CNO), leading to the conditional activation of either beta cell Gq or Gs G proteins. These newly developed transgenic mice represent powerful new tools to study G protein regulation of beta cell function in vivo.
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Direct Link:
https://nih.technologypublisher.com/tech/Transgenic_Mice_Expressing_CNO-sensi tive_Gq-_or_Gs-coupled_Designer_Receptors_Selectively_in_Pancreatic_Beta_Cells
Category(s):
Collaboration
Endocrinology
Research Materials
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For Information, Contact:
Mythreyi Shastri
Technology Development Specialist
NIH Technology Transfer
301-435-0613
shastrim@mail.nih.gov
Inventors:
Jean-Marc Guettier
Jurgen Wess
Keywords:
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Beta-RASSL-1
Beta-RASSL-2
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Mice
RIPII-RQ
RIPII-Rs
TRANSGENIC
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