Evidence map›Paper›PMID 26117324›Full record

ReviewFree radical biology & medicine2015

Signaling and stress: The redox landscape in NOS2 biology.

Douglas D Thomas, Julie L Heinecke, Lisa A Ridnour, Robert Y Cheng, Aparna H Kesarwala, Christopher H Switzer, Daniel W McVicar, David D Roberts, Sharon Glynn, Jon M Fukuto and 2 more

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 144 citations in OpenAlex.

  1. Article
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  18. Nitric Oxide Signaling and Sensing in Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2024
    Review
  19. Article
  20. Review

8 more citing papers are in PubMed but not listed here.

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

12 authors at 6 institutions in 2 countries.

Douglas D ThomasDepartment of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Illinois at Chicago, Chicago, IL 60612, USA.
Julie L HeineckeRadiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Lisa A RidnourRadiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Robert Y ChengRadiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Aparna H KesarwalaRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Christopher H SwitzerRadiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Daniel W McVicarCancer and Inflammation Program, National Cancer Institute-Frederick, Frederick, MD 21702, USA.
David D RobertsLaboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Sharon GlynnProstate Cancer Institute, NUI Galway, Ireland, USA.
Jon M FukutoDepartment of Chemistry, Sonoma State University, Rohnert Park, CA 94928, USA.
David A WinkRadiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: wink@mail.nih.gov.
Katrina M MirandaDepartment of Chemistry, University of Arizona, 1306 E. University Blvd., Tucson, AZ 85721, USA. Electronic address: kmiranda@email.arizona.edu.
National Cancer Institute · USNational Institutes of Health · USOllscoil na Gaillimhe – University of Galway · IESonoma State University · USUniversity of Arizona · USUniversity of Illinois Chicago · US

Funding

Signal Transduction of Paired Inhibitory Receptors of NK Cells and MacrophagesZIABC010300 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MCVICAR, DANIEL W. · 2009 to 2025
$24.6M
Nitric Oxide as a Modifier of Oxidative StressZIASC007281 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI WINK, DAVID · 2009 to 2025
$8.1M
Roles of Glycoconjugates and Redox Signaling in Tumor BiologyZIASC009174 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI ROBERTS, DAVID D · 2009 to 2024
$4.9M
NITRIC OXIDE AS A MODIFIER OF OXIDATIVE STRESSZ01SC007281 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI WINK, DAVID A · 1996 to 2008
$1.8M
Structure and function of chloride channels and transportersR01GM085232 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI ACCARDI, ALESSIO · 2009 to 2013
$1.7M
Assessment of the Chemical Biology of HNO via New DonorsR01GM076247 · NIGMS · UNIVERSITY OF ARIZONA · PI MIRANDA, KATRINA M. · 2006 to 2010
$1.1M
Intramural NIH HHS Z01 SC007281NIGMS NIH HHS R01 GM076247NIGMS NIH HHS R01-GM076247NIGMS NIH HHS R01 GM085232NIGMS NIH HHS R01GM085232
6 · The paper itself

Abstract

Nitric oxide (NO) has a highly diverse range of biological functions from physiological signaling and maintenance of homeostasis to serving as an effector molecule in the immune system. However, deleterious as well as beneficial roles of NO have been reported. Many of the dichotomous effects of NO and derivative reactive nitrogen species (RNS) can be explained by invoking precise interactions with different targets as a result of concentration and temporal constraints. Endogenous concentrations of NO span five orders of magnitude, with levels near the high picomolar range typically occurring in short bursts as compared to sustained production of low micromolar levels of NO during immune response. This article provides an overview of the redox landscape as it relates to increasing NO concentrations, which incrementally govern physiological signaling, nitrosative signaling and nitrosative stress-related signaling. Physiological signaling by NO primarily occurs upon interaction with the heme protein soluble guanylyl cyclase. As NO concentrations rise, interactions with nonheme iron complexes as well as indirect modification of thiols can stimulate additional signaling processes. At the highest levels of NO, production of a broader range of RNS, which subsequently interact with more diverse targets, can lead to chemical stress. However, even under such conditions, there is evidence that stress-related signaling mechanisms are triggered to protect cells or even resolve the stress. This review therefore also addresses the fundamental reactions and kinetics that initiate signaling through NO-dependent pathways, including processes that lead to interconversion of RNS and interactions with molecular targets.

Indexed as

Oxidation-ReductionApoptosisFree RadicalsHumansNeoplasmsNitric OxideNitric Oxide Synthase Type IIOxidative StressReactive Nitrogen SpeciesSignal TransductionFree RadicalsNitric OxideNitric Oxide Synthase Type IINOS2 protein, humanReactive Nitrogen SpeciesBreast cancerCancer biologyCell signalingFree radicalsNitric oxideNitric oxide synthase

Identifiers

PMID26117324
PMCPMC4852151
OpenAlexW992309826

What OpenQuestion holds

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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.