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Transcription profiling of mouse heart from Emd KO and controls

ABSTRACT: The present research is devoted to the identification of gene(s) severely affected by EMD mutations, leading to striated muscle laminopathies and more specifically the cardiomyopathy. For this purpose, we developped a large-scale gene expression approach on heart and skeletal tissues from Emd KO mouse model. Experiment Overall Design: In the project presented here we performed differential expression in heart from a mouse model of EDMD: a Emd KO mouse created via homologous recombination by Y.Hayashi in Japan (Ozawa, 2006). The emd knock-out mouse showed significantly delayed PR time, that could correspond to impaired atrial-ventricle node conduction. Genes were identified as differentially expressed if they met a false discovery rate threshold of 0.05 in a two-sample t-test (q-value) and showed at least a two-fold difference in expression independent of absolute signal intensity.

ORGANISM(S): Mus musculus

SUBMITTER: antoine Muchir

PROVIDER: E-GEOD-6399 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Activation of MAPK in hearts of EMD null mice: similarities between mouse models of X-linked and autosomal dominant Emery Dreifuss muscular dystrophy.

Muchir Antoine A Pavlidis Paul P Bonne Gisèle G Hayashi Yukiko K YK Worman Howard J HJ

Human molecular genetics 20070613 15

Emery-Dreifuss muscular dystrophy (EDMD) is an inherited disorder characterized by slowly progressive skeletal muscle weakness in a humero-peroneal distribution, early contractures and prominent cardiomyopathy with conduction block. Mutations in EMD, encoding emerin, and LMNA, encoding A-type lamins, respectively, cause X-linked and autosomal dominant EDMD. Emerin and A-type lamins are proteins of the inner membrane of the nuclear envelope. Whereas the genetic cause of EDMD has been described an ...[more]

PMID: 17567779

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Comparison between gene expression in heart from Emd KO and control mice

Project description:The present research is devoted to the identification of gene(s) severely affected by EMD mutations, leading to striated muscle laminopathies and more specifically the cardiomyopathy. For this purpose, we developped a large-scale gene expression approach on heart and skeletal tissues from Emd KO mouse model. Keywords: disease state modification

2006-12-02 | GSE6399 | GEO

Comparison between gene expression in heart from Lmna H222P homozygous and control mice

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Comparison between gene expression in heart from Lmna H222P heterozygous and control mice

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Transcription profiling of mouse heart from Lmna H222P heterozygous and control mice

Project description:The present research is devoted to the identification of gene(s) severely affected by LMNA mutations, leading to striated muscle laminopathies and more specifically the cardiomyopathy. For this purpose, we developped a large-scale gene expression approach on heart and skeletal tissues from Lmna H222P heterozygous Knock-In mouse model. Experiment Overall Design: In the project presented here we performed differential expression in heart from a mouse model of EDMD: a LmnaH222P knock-in mouse created via homologous recombination by Gisele Bonne in Paris, France (Arimura et al., 2005). The mutant male LmnaH222P knock-in homozygous mice display reduced locomotion activity with abnormal stiff walking posture and all of them die by 9 months of age. As for cardiac phenotype, they develop chamber dilation and hypokinesia with conduction defects. These results demonstrate that LmnaH222P knock-in homozygous mice represents a good model for studying laminopathies affecting striated muscles as they develop a dystrophic condition of both skeletal and cardiac muscles reminiscent of the human diseases. Genes were identified as differentially expressed if they met a false discovery rate threshold of 0.05 in a two-sample t-test (q-value) and showed at least a two-fold difference in expression independent of absolute signal intensity.

2008-06-14 | E-GEOD-6397 | biostudies-arrayexpress

Transcription profiling of heart from Lmna H222P homozygous and control mice

2008-06-14 | E-GEOD-6398 | biostudies-arrayexpress

transcriptomic data of soleus WT and Lmnap.H222P/H222P pre- and post-symptomatic mice

Project description:The present research is devoted to the identification of gene(s) severely affected by LMNA mutations, leading to striated muscle laminopathies and more specifically the skeletal phenotype of Emery-Freifuss Muscular Dystrophy. For this purpose, we developed a large-scale gene expression approach on soleus skeletal tissues from wild type Lmna H222P homozygous Knock-In mouse mode at pre and post stages of the disease .

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Function of Pitx2 in postnatal heart

Project description:Pitx2 is the homeobox gene located in proximity to the human 4q25 familial atrial fibrillation locus. Pitx2 haploinsufficient mice are prone to pacing induced atrial fibrillation indicating that reduced Pitx2 promotes an arrhythmogenic substrate within the atrium. Here, we inactivated Pitx2 in postnatal heart and discovered that unstressed adult Pitx2 mutant mice had sinus node dysfunction with impaired atrial conduction, an arrhythmia closely associated with atrial fibrillation. A genome-wide search for Pitx2 transcriptional targets using ChIP-sequencing and RNA expression profiling shows that Pitx2 represses target genes encoding cell junction proteins, ion channels, and critical transcriptional regulators many of which have been implicated in human atrial fibrillation by genome wide association studies. Our findings unveil a Pitx2 postnatal arrhythmogenic function, novel Pitx2 target genes relevant to atrial fibrillation, and reveal that Pitx2 stabilizes the intercalated disc in postnatal atrium. Genomic occupancy profiling of transcriptional factor Pitx2 in postnatal heart.

2014-02-01 | E-GEOD-47928 | biostudies-arrayexpress

ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes

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2018-10-15 | GSE115061 | GEO

Gene expression data of postnatal Pitx2 deficient heart

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2014-02-01 | E-GEOD-50399 | biostudies-arrayexpress

Genome-wide occupancy profile of Tbx3 in adult mouse whole heart

Project description:The contraction pattern of the heart relies on the activation and conduction of the electrical impulse. Perturbations of cardiac conduction have been associated with congenital and acquired arrhythmias as well as cardiac arrest. The pattern of conduction depends on the regulation of heterogeneous gene expression by key transcription factors and transcriptional enhancers. Here, we assessed the genome-wide occupation of conduction system–regulating transcription factors TBX3 in the mouse heart, uncovering cardiac enhancers throughout the genome. Examination of the cardiac transcription factor Tbx3 in adult mouse heart

2013-03-05 | E-GEOD-44821 | biostudies-arrayexpress

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