Proteomics

Dataset Information

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EndoC-betaH3 Cell FANCA Protein Interactions Regulated by Glucose Stimulation


ABSTRACT: Hyperinsulinemia affects 72% of Fanconi anemia (FA) patients and an additional 25% experience lowered glucose tolerance or frank diabetes. The underlying molecular mechanisms contributing to the dysfunction of FA pancreas β cells is unknown. Therefore, we sought to identify previously unexplored roles of FA proteins in the glucose responsive human pancreas β cell line EndoC-βH3 using a mass spectrometry-based protein interaction analysis of endogenous FANCA. This study reveals glucose stimulation-dependent changes in the FANCA interaction network indicative of the DNA damage response (DDR) through interactions with other FA proteins. We identify protein interactions with FANCA related to β cell insulin secretion.

INSTRUMENT(S): Orbitrap Fusion Lumos, Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Type B Pancreatic Cell, Endocrine Pancreas

DISEASE(S): Disease Free

SUBMITTER: Nicholas Woods  

LAB HEAD: Nicholas T. Woods

PROVIDER: PXD010589 | Pride | 2019-07-25

REPOSITORIES: Pride

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Publications

Delineating the role of FANCA in glucose-stimulated insulin secretion in β cells through its protein interactome.

Lagundžin Dragana D   Hu Wen-Feng WF   Law Henry C H HCH   Krieger Kimiko L KL   Qiao Fangfang F   Clement Emalie J EJ   Drincic Andjela T AT   Nedić Olgica O   Naldrett Michael J MJ   Alvarez Sophie S   Woods Nicholas T NT  

PloS one 20190828 8


Hyperinsulinemia affects 72% of Fanconi anemia (FA) patients and an additional 25% experience lowered glucose tolerance or frank diabetes. The underlying molecular mechanisms contributing to the dysfunction of FA pancreas β cells is unknown. Therefore, we sought to evaluate the functional role of FANCA, the most commonly mutated gene in FA, in glucose-stimulated insulin secretion (GSIS). This study reveals that FANCA or FANCB knockdown impairs GSIS in human pancreas β cell line EndoC-βH3. To ide  ...[more]

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