دورية أكاديمية
A Cellular Mechanism to Detect and Alleviate Reductive Stress.
| العنوان: | A Cellular Mechanism to Detect and Alleviate Reductive Stress. |
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| المؤلفون: | Manford AG; Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley CA 94720, USA., Rodríguez-Pérez F; Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley CA 94720, USA; Howard Hughes Medical Institute, University of California at Berkeley, Berkeley CA 94720, USA., Shih KY; Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley CA 94720, USA; Howard Hughes Medical Institute, University of California at Berkeley, Berkeley CA 94720, USA., Shi Z; Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley CA 94720, USA., Berdan CA; Department of Nutritional Science and Toxicology, University of California at Berkeley, Berkeley CA 94720, USA., Choe M; Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley CA 94720, USA; Department of Nutritional Science and Toxicology, University of California at Berkeley, Berkeley CA 94720, USA; Center for Computational Biology, University of California at Berkeley, Berkeley CA 94720, USA., Titov DV; Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley CA 94720, USA; Department of Nutritional Science and Toxicology, University of California at Berkeley, Berkeley CA 94720, USA; Center for Computational Biology, University of California at Berkeley, Berkeley CA 94720, USA., Nomura DK; Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley CA 94720, USA; Department of Nutritional Science and Toxicology, University of California at Berkeley, Berkeley CA 94720, USA; Department of Chemistry, University of California at Berkeley, CA 94720, USA., Rape M; Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley CA 94720, USA; Howard Hughes Medical Institute, University of California at Berkeley, Berkeley CA 94720, USA; California Institute for Quantitative Biosciences (QB3), University of California at Berkeley, Berkeley, CA 94720, USA. Electronic address: mrape@berkeley.edu. |
| المصدر: | Cell [Cell] 2020 Oct 01; Vol. 183 (1), pp. 46-61.e21. Date of Electronic Publication: 2020 Sep 16. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Cell Press Country of Publication: United States NLM ID: 0413066 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4172 (Electronic) Linking ISSN: 00928674 NLM ISO Abbreviation: Cell Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Cambridge, Ma : Cell Press Original Publication: Cambridge, MIT Press. |
| مواضيع طبية MeSH: | Carrier Proteins/*metabolism , Oxidative Stress/*physiology , Reactive Oxygen Species/*metabolism, Antioxidants/metabolism ; Carrier Proteins/genetics ; Cell Differentiation ; HEK293 Cells ; Homeostasis ; Humans ; Kelch-Like ECH-Associated Protein 1/metabolism ; Mitochondria ; Muscle Development/physiology ; Myoblasts/metabolism ; NF-E2-Related Factor 2/metabolism ; Signal Transduction ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination |
| مستخلص: | Metazoan organisms rely on conserved stress response pathways to alleviate adverse conditions and preserve cellular integrity. Stress responses are particularly important in stem cells that provide lifetime support for tissue formation and repair, but how these protective systems are integrated into developmental programs is poorly understood. Here we used myoblast differentiation to identify the E3 ligase CUL2 FEM1B and its substrate FNIP1 as core components of the reductive stress response. Reductive stress, as caused by prolonged antioxidant signaling or mitochondrial inactivity, reverts the oxidation of invariant Cys residues in FNIP1 and allows CUL2 FEM1B to recognize its target. The ensuing proteasomal degradation of FNIP1 restores mitochondrial activity to preserve redox homeostasis and stem cell integrity. The reductive stress response is therefore built around a ubiquitin-dependent rheostat that tunes mitochondrial activity to redox needs and implicates metabolic control in coordination of stress and developmental signaling. Competing Interests: Declaration of Interest M.R. is a co-founder and consultant to Nurix, a publicly traded company in the ubiquitin space. D.K.N. is a co-founder, shareholder, and adviser of Frontier Medicines. (Copyright © 2020 Elsevier Inc. All rights reserved.) |
| معلومات مُعتمدة: | United States HHMI Howard Hughes Medical Institute; S10 OD020062 United States OD NIH HHS; S10 OD018174 United States OD NIH HHS |
| فهرسة مساهمة: | Keywords: FEM1B; FNIP1; KEAP1; mitochondria; oxidative stress; proteasome; reactive oxygen; reductive stress; ubiquitin |
| المشرفين على المادة: | 0 (Antioxidants) 0 (Carrier Proteins) 0 (FNIP1 protein, human) 0 (Kelch-Like ECH-Associated Protein 1) 0 (NF-E2-Related Factor 2) 0 (Reactive Oxygen Species) EC 2.3.2.27 (Ubiquitin-Protein Ligases) |
| تواريخ الأحداث: | Date Created: 20200917 Date Completed: 20210517 Latest Revision: 20230928 |
| رمز التحديث: | 20230928 |
| DOI: | 10.1016/j.cell.2020.08.034 |
| PMID: | 32941802 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1097-4172 |
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| DOI: | 10.1016/j.cell.2020.08.034 |