Deletion of C/EBP homologous protein (Chop) in C57Bl/6 mice dissociates obesity from insulin resistance (Q61993990)

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20 January 2020

title

Deletion of C/EBP homologous protein (Chop) in C57Bl/6 mice dissociates obesity from insulin resistance (English)

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20 January 2020

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20 January 2020

author name string

M Maris

1

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20 January 2020

L Overbergh

2

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20 January 2020

C Gysemans

3

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20 January 2020

A Waget

4

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20 January 2020

A K Cardozo

5

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20 January 2020

E Verdrengh

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20 January 2020

J P M Cunha

7

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20 January 2020

T Gotoh

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20 January 2020

D L Eizirik

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R Burcelin

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C Mathieu

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20 January 2020

publication date

12 January 2012

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20 January 2020

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20 January 2020

volume

55

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20 January 2020

issue

4

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20 January 2020

page(s)

1167-1178

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https://scigraph.springernature.com/pub.10.1007/s00125-011-2427-7

20 January 2020

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CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum

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CCAAT/Enhancer-binding protein homologous protein (CHOP) decreases bone formation and causes osteopenia

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Chop deletion reduces oxidative stress, improves beta cell function, and promotes cell survival in multiple mouse models of diabetes

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Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance

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C/EBP homologous protein is crucial for the acceleration of experimental pancreatitis

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Suppressor of cytokine signaling 1 (SOCS-1) and SOCS-3 cause insulin resistance through inhibition of tyrosine phosphorylation of insulin receptor substrate proteins by discrete mechanisms

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Targeted disruption of the Chop gene delays endoplasmic reticulum stress-mediated diabetes

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hsp70-DnaJ chaperone pair prevents nitric oxide- and CHOP-induced apoptosis by inhibiting translocation of Bax to mitochondria

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Aberrant lipid metabolism disrupts calcium homeostasis causing liver endoplasmic reticulum stress in obesity

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Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes

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Identification of novel stress-induced genes downstream of chop

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Increase in endoplasmic reticulum stress-related proteins and genes in adipose tissue of obese, insulin-resistant individuals

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C/EBP homologous protein (CHOP) is crucial for the induction of caspase-11 and the pathogenesis of lipopolysaccharide-induced inflammation

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Adaptive suppression of the ATF4-CHOP branch of the unfolded protein response by toll-like receptor signalling

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Chop-deficient mice showed increased adiposity but no glucose intolerance.

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Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS)

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12 December 2020