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Atp-sensitive potassium channels mediate survival during infection in mammals and insects

Academic Article
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Overview

authors

  • Croker, B.
  • Crozat, K.
  • Berger, M.
  • Xia, Y.
  • Sovath, S.
  • Schaffer, L.
  • Eleftherianos, I.
  • Imler, J. L.
  • Beutler, Bruce

publication date

  • December 2007

journal

  • Nature Genetics  Journal

abstract

  • Specific homeostatic mechanisms confer stability in innate immune responses, preventing injury or death from infection. Here we identify, from a screen of N-ethyl-N-nitrosourea-mutagenized mice, a mutation causing both profound susceptibility to infection by mouse cytomegalovirus and approximately 20,000-fold sensitization to lipopolysaccharide (LPS), poly(I.C) and immunostimulatory (CpG) DNA. The LPS hypersensitivity phenotype is not suppressed by mutations in Myd88, Trif, Tnf, Tnfrsf1a, Ifnb, Ifng or Stat1, genes contributing to LPS responses, and results from an abnormality extrinsic to hematopoietic cells. The phenotype is due to a null allele of Kcnj8, encoding Kir6.1, a protein that combines with SUR2 to form an ATP-sensitive potassium channel (K(ATP)) expressed in coronary artery smooth muscle and endothelial cells. In Drosophila melanogaster, suppression of dSUR by RNA interference similarly causes hypersensitivity to infection by flock house virus. Thus, K(ATP) evolved to serve a homeostatic function during infection, and in mammals it prevents coronary artery vasoconstriction induced by cytokines dependent on TLR and/or MDA5 immunoreceptors.

subject areas

  • ATP-Binding Cassette Transporters
  • Animals
  • Cloning, Molecular
  • Coronary Vessels
  • Crosses, Genetic
  • Drosophila Proteins
  • Drosophila melanogaster
  • Ethylnitrosourea
  • Homozygote
  • Infection
  • KATP Channels
  • Lipopolysaccharides
  • Mice
  • Molecular Sequence Data
  • Mutagenesis
  • Potassium Channels, Inwardly Rectifying
  • Sulfonylurea Receptors
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Identity

International Standard Serial Number (ISSN)

  • 1061-4036

Digital Object Identifier (DOI)

  • 10.1038/ng.2007.25

PubMed ID

  • 18026101
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Additional Document Info

start page

  • 1453

end page

  • 1460

volume

  • 39

issue

  • 12

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