ArticleNeurochemical research2016
Disulfide Stress Targets Modulators of Excitotoxicity in Otherwise Healthy Brains.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
10 citing papers in PubMed, 11 citations in OpenAlex.
- Disulfidptosis: A Metabolic Cell Death Mechanism with Therapeutic Potential in Cancer.Oncology research · 2026Review
- Disulfide stress and its role in cardiovascular diseases.Redox biology · 2024Review
- Protein vicinal thiols as intrinsic probes of brain redox states in health, aging, and ischemia.Metabolic brain disease · 2024Article
- Regulation of Cardiac PKA Signaling by cAMP and Oxidants.Antioxidants (Basel, Switzerland) · 2021Review
- The Reducible Disulfide Proteome of Synaptosomes Supports a Role for Reversible Oxidations of Protein Thiols in the Maintenance of Neuronal Redox Homeostasis.Neurochemical research · 2020Article
- Reductive Reprogramming: A Not-So-Radical Hypothesis of Neurodegeneration Linking Redox Perturbations to Neuroinflammation and Excitotoxicity.Cellular and molecular neurobiology · 2019Review
- Potential widespread denitrosylation of brain proteins following prolonged restraint: proposed links between stress and central nervous system disease.Metabolic brain disease · 2019Article
- The reduced activity of PP-1α under redox stress condition is a consequence of GSH-mediated transient disulfide formation.Scientific reports · 2018Article
- Disruption of microglia histone acetylation and protein pathways in mice exhibiting inflammation-associated depression-like symptoms.Psychoneuroendocrinology · 2018Article
- Redox Signaling in Neurotransmission and Cognition During Aging.Antioxidants & redox signaling · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress is a long-hypothesized cause of diverse neurological and psychiatric disorders but the pathways by which physiological redox perturbations may detour healthy brain development and aging are unknown. We reported recently (Foley et al., Neurochem Res 39:2030-2039, 2014) that two-electron oxidations, to disulfides, of protein vicinal thiols can vary markedly in association with more modest oxidations of the glutathione redox couple in brains from healthy adolescent rats whereas levels of protein S-glutathionylation were low and unchanged. Here, we demonstrate that the selective oxidations of protein vicinal thiols, occurring only in the more oxidized brains under study, were linked specifically to a peroxide stress as evidenced by increased oxidations, to disulfides, of the presumed catalytic vicinal thiols of peroxiredoxins 1 and 2. Moreover, we identify the catalytic subunit(s) of Na
Indexed as
Identifiers
What OpenQuestion holds
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.