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Series GSE22295 Query DataSets for GSE22295
Status Public on Oct 01, 2010
Title Lack of chemokine signaling through CXCR5 causes mortality, ventricular dilatation and deranged matrix during pressure overload
Organism Mus musculus
Experiment type Expression profiling by array
Summary Inflammatory mechanisms have been suggested to play a role in the development of heart failure (HF), but a role for chemokines is largely unknown. The aim of this study was to analyze the role of the chemokine CXCL13 and its receptor CXCR5 in cardiac pathophysiology leading to HF
 
Overall design A microarray study was performed on seven mice harboring a systemic knockout of the CXCR5 (CXCR5-/-) and seven wildtype mice. Four of the knockouts and four of the wild type mice were subjected to aorta banding and three of each to sham operations.
 
Contributor(s) Wæhre A, Nygård S, Christensen G
Citation(s) 21533157
Submission date Jun 10, 2010
Last update date Mar 04, 2019
Contact name Ståle Nygård
E-mail(s) stale.nygard@medisin.uio.no
Phone +47 95129127
Organization name University of Oslo
Street address Institute for Experimental Medical Research, Oslo University Hospital - Ulleval
City Oslo
ZIP/Postal code 0407
Country Norway
 
Platforms (1)
GPL6246 [MoGene-1_0-st] Affymetrix Mouse Gene 1.0 ST Array [transcript (gene) version]
Samples (14)
GSM554832 left ventricle, aorta banding, cxcr5 knockout, rep1
GSM554833 left ventricle, aorta banding, cxcr5 knockout, rep2
GSM554834 left ventricle, aorta banding, cxcr5 knockout, rep3
Relations
BioProject PRJNA127413

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE22295_RAW.tar 53.0 Mb (http)(custom) TAR (of CEL)
Processed data included within Sample table

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