Autophagy deficiency in beta cells leads to compromised unfolded protein response and progression from obesity to diabetes in mice (Q38330390)

2 September 2017

Autophagy deficiency in beta cells leads to compromised unfolded protein response and progression from obesity to diabetes in mice (English)

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2 September 2017

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M Komatsu

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author name string

W Quan

1

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2 September 2017

K Y Hur

2

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2 September 2017

Y Lim

3

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2 September 2017

S H Oh

4

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2 September 2017

J-C Lee

5

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2 September 2017

K H Kim

6

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2 September 2017

G H Kim

7

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2 September 2017

S-W Kim

8

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2 September 2017

H L Kim

9

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2 September 2017

M-K Lee

10

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2 September 2017

K-W Kim

11

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2 September 2017

J Kim

12

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2 September 2017

M-S Lee

14

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2 September 2017

11 November 2011

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2 September 2017

55

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2 September 2017

392-403

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2 September 2017

2

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https://scigraph.springernature.com/pub.10.1007/s00125-011-2350-y

2 September 2017

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ER stress (PERK/eIF2alpha phosphorylation) mediates the polyglutamine-induced LC3 conversion, an essential step for autophagy formation.

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Autophagy is activated for cell survival after endoplasmic reticulum stress

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Endoplasmic reticulum stress triggers autophagy

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Control of mRNA translation preserves endoplasmic reticulum function in beta cells and maintains glucose homeostasis

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Endoplasmic reticulum stress contributes to beta cell apoptosis in type 2 diabetes

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Loss of autophagy diminishes pancreatic beta cell mass and function with resultant hyperglycemia

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Autophagy in human type 2 diabetes pancreatic beta cells.

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Translation attenuation through eIF2alpha phosphorylation prevents oxidative stress and maintains the differentiated state in beta cells

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A regulatory subunit of phosphoinositide 3-kinase increases the nuclear accumulation of X-box-binding protein-1 to modulate the unfolded protein response

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Real-time redox measurements during endoplasmic reticulum stress reveal interlinked protein folding functions

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Initiation and execution of lipotoxic ER stress in pancreatic beta-cells

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Autophagy proteins regulate innate immune responses by inhibiting the release of mitochondrial DNA mediated by the NALP3 inflammasome

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A decrease in cellular energy status stimulates PERK-dependent eIF2alpha phosphorylation and regulates protein synthesis in pancreatic beta-cells

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NF-kappa B prevents beta cell death and autoimmune diabetes in NOD mice

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Autophagy is important in islet homeostasis and compensatory increase of beta cell mass in response to high-fat diet

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Ubiquitin fold modifier 1 (UFM1) and its target UFBP1 protect pancreatic beta cells from ER stress-induced apoptosis

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PubMed

https://pubmed.ncbi.nlm.nih.gov/22075916

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Transactivation of the grp78 promoter by Ca2+ depletion. A comparative analysis with A23187 and the endoplasmic reticulum Ca(2+)-ATPase inhibitor thapsigargin

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/22075916

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Apoptosis of pancreatic beta-cells detected in accelerated diabetes of NOD mice: no role of Fas-Fas ligand interaction in autoimmune diabetes

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/22075916

inferred from PubMed ID database lookup

12 December 2020

based on heuristic

Identifiers

DOI

10.1007/S00125-011-2350-Y

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Dimensions Publication ID

2 September 2017

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1 reference