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Cited by 281Neutrophil, Myeloperoxidase and Oxidative MechanismsImmunodeficiency and Autoimmune DisordersRedox biology and oxidative stress

Stimulated neutrophils from patients with autosomal recessive chronic granulomatous disease fail to phosphorylate a Mr-44,000 protein

Segal, Anthony W., Heyworth, Paul G., Cockcroft, Shamshad, Barrowman, Margaret M.·1985·Nature
DOI 10.1038/316547a0
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Abstract

Phagocytosing neutrophils, monocytes, macrophages and eosinophils produce a burst of non-mitochondrial respiration that is important for the killing and digestion of microbes. Much of the information about the oxidase system involved comes from studies on patients with chronic granulomatous disease (CGD), a syndrome in which an undue predisposition to infection results from complete absence of this burst of stimulated respiratory activity. The basis of the oxidase activity is an electron transport chain, the only established component of which is a very unusual b-type cytochrome (b-245) (ref. 2). The molecular defect in the X-linked subgroup of CGD is the absence of this cytochrome b-245, which, however, appears to be normal in those subjects with the autosomal recessive mode of inheritance. In an attempt to identify an abnormality of activation, or an absence or malfunction of a proximal component of the electron transport chain in this latter group, we examined protein phosphorylation in neutrophils after activation of the oxidase with phorbol myristate acetate. All four of the patients studied demonstrated a selective lack of the enhanced phosphorylation of a protein of relative molecular mass (Mr) 44,000 (44K) that was observed in normal subjects and in two CGD patients with an X-linked inheritance. This molecule, therefore, could be an important functional component of the oxidase.

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  • H2O2 can modulate gene expression by epigenetic modification and activate transcription factors such as AP-1, NRF2, CREB, HSF1, HIF-1, TP53, NF-κβ, NOTCH, SP1, SCREB-1 and FOXO family.

    “For example, H2O2 can also modulate genes expression by epigenetic modification and activate transcription factors such as AP-1, NRF2, CREB, HSF1, HIF-1, TP53, NF-κβ, NOTCH, SP1, SCREB-1 and FOXO family [14,15,16,17,18,19,20,21,22].”

    From The Role of Reactive Species on Innate Immunity (2022) · cites this paper as [18]

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Authors
Segal, A. W., Heyworth, P. G., Cockcroft, S., & Barrowman, M. M.
Affiliations
University College London (GB)
ORCID
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
1985-08
Volume
316
Issue
6028
Pages
547-549
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
DOI
10.1038/316547a0
OpenAlex
W1984457008
Cited by
281
References
19
Citations by year
2026: 3 · 2023: 6 · 2022: 2 · 2021: 1 · 2019: 2 · 2018: 2 · 2017: 3 · 2016: 3 · 2015: 1 · 2014: 1 · 2013: 3
FWCI
9.09
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords
chronic granulomatous disease, autosomal recessive inheritance, neutrophils, protein phosphorylation, NADPH oxidase, electron transport chain, phorbol myristate acetate, non-mitochondrial respiration, X-linked CGD, respiratory burst
MeSH terms
Genes, Recessive, Granulomatous Disease, Chronic, Humans, Membrane Proteins, Molecular Weight, Neutrophils, Oxidoreductases, Phosphoproteins, Phosphorylation, Tetradecanoylphorbol Acetate

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