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Transcription profiling of mouse heart from embryonic day 9.5 from Nkx2.5 deleted mice, Nkx.5 is a mouse model of congenital heart disease

ABSTRACT: We have developed gene-targeted mice with deletion of Nkx2.5. Embryos were isolated at embryonic day 9.5 and the middle third containing the heart was run on Affymetrix Mu11kA and Mu11kB arrays. For more information about this model see; http://cardiogenomics.med.harvard.edu/groups/proj1/pages/csx_home.html

ORGANISM(S): Mus musculus

DISEASE(S): cogenital heart disease

SUBMITTER: Martina Schinke

PROVIDER: E-GEOD-78 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Congenital heart disease in Csx/ Nkx2.5 mutant embryos

Project description:We have developed gene-targeted mice with deletion of Nkx2.5. Embryos were isolated at embryonic day 9.5 and the middle third containing the heart was run on Affymetrix Mu11kA and Mu11kB arrays. For more information about this model see http://cardiogenomics.med.harvard.edu/groups/proj1/pages/csx_home.html Keywords = Congenital heart disease Keywords: other

2002-08-02 | GSE78 | GEO

Transcription profiling of heart ventricles from mice that have cardiac hypertrophy induced by swimming training to study the molecular mechanism of exercise induced hypertrophy.

Project description:The Affymetrix GeneChip MgU74Av2 was used to analyze expression profiles of mice that had cardiac hypertrophy induced by swimming training. More information of this model can be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/swim_home.html

2007-12-19 | E-GEOD-77 | biostudies-arrayexpress

Transcription profiling of heart ventricles from mice at different developmental stages to monitor changes in cardiac gene expression over time.

Project description:The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different developmental stages to monitor changes in cardiac gene expression over time. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/fvb_home.html

2007-12-15 | E-GEOD-75 | biostudies-arrayexpress

Transcription profiling of hearts from Nkx2.5 knockout mice (mouse model of congenital heart disease) at embryonic day 12.5 shows Nkx2.5 is not only crucial during early steps of cardiogenesis but also plays an important role at later developmental stages

Project description:The NK2 family of homeobox genes constitutes a family of transcription factors that play an important role in different developmental processes. Members of this group are characterized by two highly conserved protein domains: the homeodomain, conferring DNA binding activity, and the NK2-specific domain (NK2-SD) of yet unknown function. One of the best characterized members of this group is the early cardiogenic marker Nkx2.5. Loss of function of Nkx2.5 leads to embryonic lethality around E10.5 due to an arrest of heart development at the looping stage. We have further dissected the function of Nkx2.5 in vivo by creating a knockout mouse line harboring an in frame deletion of the NK2-SD by Cre/loxP mediated excision. Homozygous mutant mice die at E14.5 due to severe cardiac malformations, e.g. common AV canal, DORV, and VSD. Lack of the NK2-SD leads to downregulation of the ventricular markers MLC-2v and Irx4 specifically in the right ventricle, and is accompanied with reduced right ventricular function. This function of Nkx2.5 seems to be independent of its ability to bind target DNA, since lack of the NK2-SD does not alter the DNA binding activity of Csx/Nkx2.5 in vitro. Heterozygous mutant mice show a spectrum of cardiac defects related to cardiac septation and valve morphogenesis, but lack conduction system defects as reported for heterozygous Nkx2.5 mice. The phenotype observed in NK2-SD mutant mice shows that Nkx2.5 is not only crucial during early steps of cardiogenesis but also plays an important role at later developmental stages. Embryos were isolated at embryonic day 12.5. The entire embryo heart was taken and isolated in ice-cold PBS and immediately frozen on dry-ice. Total RNA was extracted from pooled samples of wildtype, heterozygous and mutant embryos.

2007-12-13 | E-GEOD-528 | biostudies-arrayexpress

NK2 model of congenital heart disease

Project description:Lack of the conserved NK2-domain of the cardiac transcription factor Nkx2.5 causes multiple heart defects . The NK2 family of homeobox genes constitutes a family of transcription factors that play an important role in different developmental processes. Members of this group are characterized by two highly conserved protein domains: the homeodomain, conferring DNA binding activity, and the NK2-specific domain (NK2-SD) of yet unknown function. One of the best characterized members of this group is the early cardiogenic marker Nkx2.5. Loss of function of Nkx2.5 leads to embryonic lethality around E10.5 due to an arrest of heart development at the looping stage. We have further dissected the function of Nkx2.5 in vivo by creating a knockout mouse line harboring an in frame deletion of the NK2-SD by Cre/loxP mediated excision. Homozygous mutant mice die at E14.5 due to severe cardiac malformations, e.g. common AV canal, DORV, and VSD. Lack of the NK2-SD leads to downregulation of the ventricular markers MLC-2v and Irx4 specifically in the right ventricle, and is accompanied with reduced right ventricular function. This function of Nkx2.5 seems to be independent of its ability to bind target DNA, since lack of the NK2-SD does not alter the DNA binding activity of Csx/Nkx2.5 in vitro. Heterozygous mutant mice show a spectrum of cardiac defects related to cardiac septation and valve morphogenesis, but lack conduction system defects as reported for heterozygous Nkx2.5 mice. The phenotype observed in NK2-SD mutant mice shows that Nkx2.5 is not only crucial during early steps of cardiogenesis but also plays an important role at later developmental stages. Embryos were isolated at embryonic day 12.5. The entire embryo heart was taken and isolated in ice-cold PBS and immediately frozen on dry-ice. Total RNA was extracted from pooled samples of wildtype, heterozygous and mutant embryos. Keywords = congenital heart disease, Csx, Nkx2.5 Keywords: other

2003-07-13 | GSE528 | GEO

Transcription profiling of heart ventricles from 10 week old mice heterozygous for dn-p21ras and 3 month old wild type FVB mice to study severe dilated cardiomyopathy.

Project description:Mice heterozygous for dn-p21 littermates were sacrificed at 10 weeks of age. Ventricles were isolated and snap-frozen in liquid nitrogen. Use 3 month old FVB Females as controls. [GSM2334, GSM2335, GSM2336]; Read more at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/ras_home.html

2007-12-15 | E-GEOD-760 | biostudies-arrayexpress

Transcription profiling of heart ventricles from mice at different time points after surgical intervention for pressure-overload induced hypertrophy to identify differentially expressed genes.

Project description:Aortic banding is an excellent model system to evaluate the process of development of left ventricular hypertrophy in response to hemodynamic stress. The Affymetrix GeneChip MgU74Av1 was used to analyze expression profiles of mice at different time points after surgical intervention for pressure-overload induced hypertrophy. More information about this model may be obtained at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/band_home.html

2007-12-19 | E-GEOD-76 | biostudies-arrayexpress

Exercised Induced Hypertrophy

2002-08-02 | GSE77 | GEO

FVB Benchmark Set for Cardiac Development, Maturation, and Aging

2002-07-30 | GSE75 | GEO

Overexpression of dn-p21ras as a model system for severe dilated cardiomyopathy

Project description:Mice heterozygous for dn-p21 littermates were sacrificed at 10 weeks of age. Ventricles were isolated and snap-frozen in liquid nitrogen. Use 3 month old FVB Females as controls. [GSM2334, GSM2335, GSM2336] Read more at http://cardiogenomics.med.harvard.edu/groups/proj1/pages/ras_home.html Keywords = ras Keywords = dilated cardiomyopathy Keywords: other

2003-10-24 | GSE760 | GEO

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