Evidence map›Paper›PMID 21803124›Full record

ReviewBiochimica et biophysica acta2012

Protein S-nitrosylation: role for nitric oxide signaling in neuronal death.

Neelam Shahani, Akira Sawa

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.4field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 57 citations in OpenAlex.

  1. Stress-induced nuclear GAPDH: Scientific update and clinical application.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  2. Review
  3. Identification of Protein Targets ofACS chemical biology · 2024
    Article
  4. Review
  5. Nitrative Stress and Auditory Dysfunction.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Nitric Oxide Synthase Inhibitors into the Clinic at Last.Handbook of experimental pharmacology · 2021
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Neelam ShahaniDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. nshahan1@jhmi.edu
Akira Sawa
Johns Hopkins Medicine · US

Funding

Research Center for Molecular Pathogenesis of SchizophreniaP20MH084018 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2008 to 2010
$3.3M
Nuclear pathway of DISC1 in major mental illnesses: biochemistry and cell biologyR01MH069853 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2004 to 2012
$3.2M
Defining of Neurodevelopmental Pathways Regulated by Neuregulin- DISC1 InteractioRC1MH088753 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ANTON, EVA S, SAWA, AKIRA · 2009 to 2010
$933k
PICK1 knockout mice: role for D-serine in neonatal forebrainsR21MH085226 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2010 to 2011
$369k
NIMH NIH HHS MH-069853NIMH NIH HHS MH-084018NIMH NIH HHS MH-085226NIMH NIH HHS MH-088753NIMH NIH HHS P20 MH084018NIMH NIH HHS R01 MH069853NIMH NIH HHS R21 MH085226NIMH NIH HHS RC1 MH088753
6 · The paper itself

Abstract

backgroundOne of the signaling mechanisms mediated by nitric oxide (NO) is through S-nitrosylation, the reversible redox-based modification of cysteine residues, on target proteins that regulate a myriad of physiological and pathophysiological processes. In particular, an increasing number of studies have identified important roles for S-nitrosylation in regulating cell death. SCOPE OF REVIEW: The present review focuses on different targets and functional consequences associated with nitric oxide and protein S-nitrosylation during neuronal cell death. MAJOR

conclusionsS-Nitrosylation exhibits double-edged effects dependent on the levels, spatiotemporal distribution, and origins of NO in the brain: in general Snitrosylation resulting from the basal low level of NO in cells exerts anti-cell death effects, whereas S-nitrosylation elicited by induced NO upon stressed conditions is implicated in pro-cell death effects. GENERAL SIGNIFICANCE: Dysregulated protein S-nitrosylation is implicated in the pathogenesis of several diseases including degenerative diseases of the central nervous system (CNS). Elucidating specific targets of S-nitrosylation as well as their regulatory mechanisms may aid in the development of therapeutic intervention in a wide range of brain diseases.

Indexed as

Cell DeathAnimalsCaspasesCell CommunicationCentral Nervous SystemCysteineHumansNeurodegenerative DiseasesNeuronsNitric OxideNitrosationOxidative StressSignal TransductionCaspasesCysteineNitric Oxide

Identifiers

PMID21803124
PMCPMC3251724
OpenAlexW2082198669

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.