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GRK2 deficiency confers cardioprotective profile.

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE41706: Expression data from adult (9 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates GSE41807: Expression data from adult (9 month-old) and young (4 month-old) hearts from C57BL/6J mice GSE41808: Expression data from adult (9 month-old) and young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice. GSE41809: Expression data from young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Lucas Elisa

PROVIDER: E-GEOD-41810 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Mus musculus

Project description:Expression data from adult (9 month-old) and young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice.

| PRJNA178239 | ENA

Expression data from adult (9 month-old) and young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice.

Project description:G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection in GRK2 hemizygous mice with age. 9 month-old and 4 month-old mice hearts were collected for RNA extraction and hybridization on Affymetrix microarrays.

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Expression data from adult (9 month-old) and young (4 month-old) hearts from C57BL/6J mice

Project description:G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection with age in GRK2 hemizygous mice in comparation with their wild-type littermates. 9 month-old and 4 month-old mice hearts were collected for RNA extraction and hybridization on Affymetrix microarrays.

2012-10-25 | E-GEOD-41807 | biostudies-arrayexpress

Expression data from adult (9 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates

Project description:G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection in GRK2 hemizygous mice. 9 month-old mice hearts were collected for RNA extraction and hybridization on Affymetrix microarrays.

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Expression data from young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates

Project description:G protein-coupled receptor kinase 2 (GRK2) has emerged as a key regulator of cardiac function and myocardial structure. Cardiac GRK2 is increased in heart failure and ischemia in humans, whereas genetic inhibition of GRK2 is cardioprotective in animal models of these pathologies. However, the mechanistic basis underlying these effects are not fully understood. We have used adult GRK2 hemizygous mice (GRK2+/-) as a model to assess the effects of a sustained systemic inhibition of GRK2 in heart tissue with age. We used microarrays to determine the global programme of gene expression underlying cardioprotection in GRK2 hemizygous mice. 4 month-old mice hearts were collected for RNA extraction and hybridization on Affymetrix microarrays.

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Project description:Expression data from young (4 month-old) hearts from GRK2 heterozygous C57BL/6J mice and its wild type littermates

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Project description:Expression data from adult (9 month-old) and young (4 month-old) hearts from C57BL/6J mice

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