CoChat
Sign Up
Cited by 246Neutrophil, Myeloperoxidase and Oxidative MechanismsRedox biology and oxidative stressImmune Response and Inflammation

The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.

NRROS negatively regulates reactive oxygen species during host defence and autoimmunity

Noubade, Rajkumar, Wong, Kit, Ota, Naruhisa, Rutz, Sascha, Eidenschenk, Celine, Valdez, Patricia A., Ding, Jiabing, Peng, Ivan, Sebrell, Andrew, Caplazi, Patrick, DeVoss, Jason, Soriano, Robert H., Sai, Tao, Lu, Rongze, Modrusan, Zora, Hackney, Jason, Ouyang, Wenjun·2014·Nature
DOI 10.1038/nature13152
Open this paper in CoChat — free account

Abstract

Reactive oxygen species (ROS) produced by phagocytes are essential for host defence against bacterial and fungal infections. Individuals with defective ROS production machinery develop chronic granulomatous disease. Conversely, excessive ROS can cause collateral tissue damage during inflammatory processes and therefore needs to be tightly regulated. Here we describe a protein, we termed negative regulator of ROS (NRROS), which limits ROS generation by phagocytes during inflammatory responses. NRROS expression in phagocytes can be repressed by inflammatory signals. NRROS-deficient phagocytes produce increased ROS upon inflammatory challenges, and mice lacking NRROS in their phagocytes show enhanced bactericidal activity against Escherichia coli and Listeria monocytogenes. Conversely, these mice develop severe experimental autoimmune encephalomyelitis owing to oxidative tissue damage in the central nervous system. Mechanistically, NRROS is localized to the endoplasmic reticulum, where it directly interacts with nascent NOX2 (also known as gp91(phox) and encoded by Cybb) monomer, one of the membrane-bound subunits of the NADPH oxidase complex, and facilitates the degradation of NOX2 through the endoplasmic-reticulum-associated degradation pathway. Thus, NRROS provides a hitherto undefined mechanism for regulating ROS production--one that enables phagocytes to produce higher amounts of ROS, if required to control invading pathogens, while minimizing unwanted collateral tissue damage.

Overview

Integrity signals

Registry

Crossref · 10.1038/nature13152

Cites

39 of 39 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Show all 39 references

Research works printed but not linked: 2

  1. DeLeo, F. R. et al. Processing and maturation of flavocytochrome b558 include incorporation of heme as a prerequisite for heterodimer assembly. J. Biol. Chem. 275, 13986–13993 (2000) · DOI
  2. Nikić, I. et al. A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis. Nature Med. 17, 495–499 (2011) · DOI · Paper page

Cited by

Sorted by citations

See all 246

Related

Metadata

Authors
Noubade, R., Wong, K., Ota, N., Rutz, S., Eidenschenk, C., Valdez, P. A., Ding, J., Peng, I., Sebrell, A., Caplazi, P., DeVoss, J., Soriano, R. H., Sai, T., Lu, R., Modrusan, Z., Hackney, J., & Ouyang, W.
Affiliations
Genentech (US)
Corresponding author
Ouyang, Wenjun
ORCID
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
2014-04-13
Volume
509
Issue
7499
Pages
235-239
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
DOI
10.1038/nature13152
OpenAlex
W2090106964
Cited by
246
References
39
Citations by year
2026: 13 · 2025: 21 · 2024: 20 · 2023: 22 · 2022: 18 · 2021: 18 · 2020: 24 · 2019: 22 · 2018: 20 · 2017: 21 · 2016: 25 · 2015: 15 · 2014: 7
FWCI
10.35
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
reactive oxygen species, NADPH oxidase, NOX2, gp91phox, endoplasmic reticulum, ER-associated degradation, phagocytes, host defense, autoimmunity, experimental autoimmune encephalomyelitis, Escherichia coli, Listeria monocytogenes, collateral tissue damage, inflammation, leucine-rich repeat proteins
MeSH terms
Animals, Bone Marrow Cells, Central Nervous System, Encephalomyelitis, Autoimmune, Experimental, Endoplasmic Reticulum, Escherichia coli, Female, Inflammation, Listeria monocytogenes, Macrophages, Male, Membrane Proteins, Oxidation-Reduction, Phagocytes, Proteins, Autoimmunity, Reactive Oxygen Species, Oxidative Stress, NADPH Oxidases, Mice, Latent TGF-beta Binding Proteins

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review