Proteomics

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Genetic predisposition for beta cell fragility underlies type 1 and type 2 diabetes


ABSTRACT: Type 1 and type 2 diabetes (T1D and T2D) share pathophysiological characteristics, yet mechanistic links have remained elusive. T1D results from autoimmune destruction of pancreatic beta cells, while beta cell failure in T2D is delayed and progressive. Here we find a new genetic component of diabetes susceptibility in T1D non-obese diabetic (NOD) mice, identifying immune-independent beta cell fragility. Genetic variation in Xrcc4 and Glis3 alter the response of NOD beta cells to unfolded protein stress, enhancing the apoptotic and senescent fates. The same transcriptional relationships were observed in human islets, demonstrating the role for beta cell fragility in genetic predisposition to diabetes.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Pancreatic Islet

SUBMITTER: Jonathan Vandenbussche  

LAB HEAD: Kris Gevaert

PROVIDER: PXD000859 | Pride | 2016-02-24

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
V17282_3346_Liston_shotgun1_1.raw Raw
V17283_3346_Liston_shotgun1_2.raw Raw
V17284_3346_Liston_shotgun1_3.raw Raw
V17285_3346_Liston_shotgun1_4.raw Raw
V17286_3346_Liston_shotgun1_5.raw Raw
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Publications


Type 1 (T1D) and type 2 (T2D) diabetes share pathophysiological characteristics, yet mechanistic links have remained elusive. T1D results from autoimmune destruction of pancreatic beta cells, whereas beta cell failure in T2D is delayed and progressive. Here we find a new genetic component of diabetes susceptibility in T1D non-obese diabetic (NOD) mice, identifying immune-independent beta cell fragility. Genetic variation in Xrcc4 and Glis3 alters the response of NOD beta cells to unfolded protei  ...[more]

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