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Related Experiment Videos

Multidomain flavin-dependent sulfhydryl oxidases.

Donald L Coppock1, Colin Thorpe

  • 1Coriell Institute for Medical Research, Camden, New Jersey, USA.

Antioxidants & Redox Signaling
|May 9, 2006
PubMed
Summary
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Quiescin sulfhydryl oxidases (QSOX) are crucial for oxidative protein folding in eukaryotes. This review highlights QSOX

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Eukaryotic flavin-dependent sulfhydryl oxidases catalyze oxidative protein folding, generating disulfides and reducing oxygen to hydrogen peroxide.
  • Quiescin sulfhydryl oxidases (QSOX) are found in multiple forms in multicellular organisms and singly in protozoan parasites.
  • QSOX proteins are ancient fusions of thioredoxin domains and an FAD-binding module (ERV1/ALR).

Purpose of the Study:

  • To review the structure, mechanism, and function of Quiescin sulfhydryl oxidases (QSOX).
  • To discuss the in vitro substrate specificity and likely in vivo substrates of QSOXs.
  • To examine the association of QSOX expression with cell types and its potential role in type II diabetes.

Main Methods:

  • Review of existing literature on QSOX structure, function, and expression.

Related Experiment Videos

  • Analysis of QSOX immunoreactivity and mRNA expression levels in human cells and tissues.
  • Comparison of QSOX proteins with related enzymes like yeast ERV1p, ERV2p, and mammalian ALR.
  • Main Results:

    • Interdomain disulfide exchanges in QSOX transmit reducing equivalents from substrates to the flavin cofactor and oxygen.
    • QSOX1 expression is strongly associated with cell types having a high secretory load of disulfide-containing proteins.
    • Abundance of sulfhydryl oxidases in islets of Langerhans suggests a role in oxidative stress linked to type II diabetes.

    Conclusions:

    • QSOX proteins play a significant role in oxidative protein folding across various organisms.
    • QSOX1 expression patterns suggest a specialized function in secretory pathways.
    • Further investigation into QSOX's role in oxidative stress and type II diabetes is warranted.