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- W3021575031 endingPage "101116" @default.
- W3021575031 startingPage "101116" @default.
- W3021575031 abstract "Many metabolic diseases disrupt endoplasmic reticulum (ER) homeostasis, but little is known about how metabolic activity is communicated to the ER. Here, we show in hepatocytes and other metabolically active cells that decreasing the availability of substrate for the tricarboxylic acid (TCA) cycle diminished NADPH production, elevated glutathione oxidation, led to altered oxidative maturation of ER client proteins, and attenuated ER stress. This attenuation was prevented when glutathione oxidation was disfavored. ER stress was also alleviated by inhibiting either TCA-dependent NADPH production or Glutathione Reductase. Conversely, stimulating TCA activity increased NADPH production, glutathione reduction, and ER stress. Validating these findings, deletion of the Mitochondrial Pyruvate Carrier-which is known to decrease TCA cycle activity and protect the liver from steatohepatitis-also diminished NADPH, elevated glutathione oxidation, and alleviated ER stress. Together, our results demonstrate a novel pathway by which mitochondrial metabolic activity is communicated to the ER through the relay of redox metabolites." @default.
- W3021575031 created "2020-05-13" @default.
- W3021575031 creator A5029688659 @default.
- W3021575031 creator A5046641549 @default.
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- W3021575031 creator A5058481769 @default.
- W3021575031 creator A5075010024 @default.
- W3021575031 creator A5075965327 @default.
- W3021575031 creator A5080467320 @default.
- W3021575031 creator A5090313762 @default.
- W3021575031 date "2020-05-01" @default.
- W3021575031 modified "2023-10-16" @default.
- W3021575031 title "NADPH and Glutathione Redox Link TCA Cycle Activity to Endoplasmic Reticulum Homeostasis" @default.
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