Reactive oxygen species control protein degradation at the mitochondrial import gate.

Rachael McMinimy, Andrew G Manford, Christine L Gee, Srividya Chandrasekhar, Gergey Alzaem Mousa, Joelle Chuang, Lilian Phu, Karen Y Shih, Christopher M Rose, John Kuriyan, Baris Bingol, Michael Rapé

Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, CA 94720, USA. · pubmed

Paper

Abstract

While reactive oxygen species (ROS) have long been known to drive aging and neurodegeneration, their persistent depletion below basal levels also disrupts organismal function. Cells counteract loss of basal ROS via the reductive stress response, but the identity and biochemical activity of ROS sensed by this pathway remain unknown. Here, we show that the central enzyme of the reductive stress response, the E3 ligase Cullin 2-FEM1 homolog B (CUL2

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the role of reactive oxygen species (ROS) in cellular function and their connection to the reductive stress response, which is relevant to understanding the mechanisms of aging and potential interventions. However, the findings appear to be more focused on biochemical pathways rather than directly addressing root causes of aging or lifespan extension. Thus, while it contributes to the field, its impact is limited.

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