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

By B. Song, D. Scheuner, D. Ron, S. Pennathur, R. Kaufman. Journal of Clinical Investigation, 2008

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The C/EBP Homologous Protein (CHOP) Transcription Factor Functions in Endoplasmic Reticulum Stress-Induced Apoptosis and Microbial Infection (2019, background): “In some models of diabetes, the deletion of CHOP can inhibit the apoptosis of pancreatic beta cells, and provides a protective mechanism to reduce the production of ERO1α, which subsequently reduces markers of oxidative stress and the expression of antioxidant genes (90).”
Endoplasmic Reticulum Stress in Liver Disease (2010, background): “Intriguingly, protein misfolding in the ER can lead to oxidative stress; and antioxidant treatment, Chop deletion, or translation attenuation can reduce oxidative stress and preserve ER function [3,89,127].”
The impact of the unfolded protein response on human disease (2012, background): “The cytotoxic effects of CHOP are at least in part through GADD34 because CHOP and GADD34 knockout animals are protected from ER stress–induced tissue damage (Marciniak et al., 2004; Malhotra et al., 2008; Song et al., 2008).”
Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, neutral): “When Chop-deficient animals are crossed with db/db mice (an extreme obesity and diabetes model characterized by the rapid demise of b cells), the death of b cells is prevented (Song et al., 2008).”
Role of Oxidative Stress in Pathophysiology of Nonalcoholic Fatty Liver Disease (2018, background): “Lastly, it activates the cellular death signaling [48].”