Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse Kir6.1-deficient heart following LPS challenge

ABSTRACT: KATP opposes depolarization of cells in the heart, smooth muscle, and other tissues by permitting the efflux of potassium ions and this efflux is evidently required to prevent unopposed vasoconstriction and insufficiency of coronary artery blood flow triggered by one or more cytokines induced in response to LPS. The cytokine(s) involved must elicit a dysfunctional response in the Kir6.1-deficient environment, and to gain further insight into the effects of the mutation, we examined the transcriptional status of whole heart, isolated from normal C57BL/6J mice or KcnJ8Md/Md mice, before and after injection of 1 μg of LPS Experiment Overall Design: 3 mice per genotype were injected with 0.5 ug LPS in PBS or with PBS alone and hearts were collected after 30 min or 3 h.

ORGANISM(S): Mus musculus

SUBMITTER: Yu Xia 

PROVIDER: E-GEOD-7605 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

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

Croker Ben B   Crozat Karine K   Berger Michael M   Xia Yu Y   Sovath Sosathya S   Schaffer Lana L   Eleftherianos Ioannis I   Imler Jean-Luc JL   Beutler Bruce B  

Nature genetics 20071118 12

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,  ...[more]

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