Article

The protection of Gα <sub>z</sub> -null NOD mice from hyperglycemia is sexually dimorphic and only partially β-cell autonomous

2021-02-09

Abstract excerpt

The mechanisms that underlie the β-cell pathophysiology of Type 1 Diabetes (T1D) are not fully understood. Our group has defined the unique heterotrimeric G protein alpha-subunit, Gα z , as a key negative regulator of β-cell signal transduction pathways. Non-obese diabetic (NOD) mice lacking Gα z throughout the body are protected from developing T1D-like hyperglycemia. To determine whether this phenotype is β-ce...

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Literature Corpus work: b834d459-1bbb-5ae5-ba2b-2d4789981e12
DOI: 10.1101/2021.02.08.430304

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