ArticleAging2009
Identification of Peroxiredoxin 1 as a novel interaction partner for the lifespan regulator protein p66Shc.
Article in Aging, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Prognostic Value of Peroxiredoxin-1 Expression in Patients with Solid Tumors: a Meta-Analysis of Cohort Study.Disease markers · 2021Pooled it
- The interplay of ferroptosis and oxidative stress in the pathogenesis of aortic dissection.Frontiers in pharmacology · 2025Review
- p66Shc in Cardiovascular Pathology.Cells · 2022Review
- Peroxiredoxin, Senescence, and Cancer.Cells · 2022Review
- Peroxiredoxin-1 Tyr194 phosphorylation regulates LOX-dependent extracellular matrix remodelling in breast cancer.British journal of cancer · 2021Article
- Specificity of Human Sulfiredoxin for Reductant and Peroxiredoxin Oligomeric State.Antioxidants (Basel, Switzerland) · 2021Article
- Peroxiredoxins wear many hats: Factors that fashion their peroxide sensing personalities.Redox biology · 2021Review
- CB1 receptor antagonist rimonabant protects against chronic intermittent hypoxia-induced renal injury in rats.BMC nephrology · 2021Article
- Dietary supplementation with ketoacids protects against CKD-induced oxidative damage and mitochondrial dysfunction in skeletal muscle of 5/6 nephrectomised rats.Skeletal muscle · 2018Article
- Peroxiredoxin Involvement in the Initiation and Progression of Human Cancer.Antioxidants & redox signaling · 2018Review
- Global analysis of erythroid cells redox status reveals the involvement of Prdx1 and Prdx2 in the severity of beta thalassemia.PloS one · 2018Article
- Sulfonation of the resolving cysteine in human peroxiredoxin 1: A comprehensive analysis by mass spectrometry.Free radical biology & medicine · 2017Article
- Peroxiredoxin 1 - an antioxidant enzyme in cancer.Journal of cellular and molecular medicine · 2017Review
- Using mitochondrial sirtuins as drug targets: disease implications and available compounds.Cellular and molecular life sciences : CMLS · 2016Review
- Fish Peroxiredoxins and Their Role in Immunity.Biology · 2015Review
- Sequence analysis, expression profiles and function of thioredoxin 2 and thioredoxin reductase 1 in resistance to nucleopolyhedrovirus in Helicoverpa armigera.Scientific reports · 2015Article
- Mitochondrial ROS Metabolism: 10 Years Later.Biochemistry. Biokhimiia · 2015Review
- Hitting the Bull's-Eye in Metastatic Cancers-NSAIDs Elevate ROS in Mitochondria, Inducing Malignant Cell Death.Pharmaceuticals (Basel, Switzerland) · 2015Review
- Acute exercise induced mitochondrial H₂O₂ production in mouse skeletal muscle: association with p(66Shc) and FOXO3a signaling and antioxidant enzymes.Oxidative medicine and cellular longevity · 2015Article
- Regulation of PRDX1 peroxidase activity by Pin1.Cell cycle (Georgetown, Tex.) · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damage caused by reactive oxygen species (ROS) contributes to many aging processes and accompanying diseases. ROS are toxic side products of cellular respiration, but also function as signal, e.g. in the mitochondrial apoptosis pathway. The protein p66Shc, which has been implicated in life-span regulation and aging-related diseases, is a central player in stress-induced apoptosis and the associated ROS burst. Stress signals, such as UV radiation or ROS themselves, activate p66Shc, which was proposed to stimulate its H(2)O(2) forming activity, ultimately triggering mitochondrial disintegration. However, mechanistic details of H(2)O(2) formation and apoptosis induction by p66Shc and regulation of these activities remain to be revealed. Here, we describe the effects of Ser36 phosphorylation and Pin1 binding on p66Shc activity, and the identification of Peroxiredoxin 1 (Prx1) as a novel interaction partner for the unique p66Shc N-terminal domain. Prx1 was identified in affinity experiments as dominant interaction partner. Complex formation leads to disassembly of Prx1 decamers, which is known to increase its peroxidase activity. The interaction leads to reduction of the p66CH2CB tetramer, which reduces its ability to induce mitochondrial rupture. Our results indicate that p66CH2CB and Prx1 form a stress-sensing complex that keeps p66Shc inactive at moderate stress levels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.