Similar studies for GEO DataSets (Select 200142125) - GEO DataSets

Select item 2001421251.

Inhibition of BRD4 Partially Rescues Dilated Cardiomyopathy and Cardiac Arrhythmias in Myocyte-Specific Lamin A/C Null Mice [RNA-Seq]

(Submitter supplied) Deletion of Lmna, encoding nuclear membrane protein LMNA, specifically in mouse cardiac myocytes activates BRD4 and leads to heart failure, arrhythmias, myocardial fibrosis, apoptosis, and premature death, which were partially rescued upon inhibition of BRD4.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL21103
12 Samples

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Series

Accession:: GSE142125

ID:: 200142125

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Select item 2001421292.

Inhibition of BRD4 Partially Rescues Dilated Cardiomyopathy and Cardiac Arrhythmias in Myocyte-Specific Lamin A/C Null Mice

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL21103 GPL21493
28 Samples

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Series

Accession:: GSE142129

ID:: 200142129

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Select item 2001421273.

Inhibition of BRD4 Partially Rescues Dilated Cardiomyopathy and Cardiac Arrhythmias in Myocyte-Specific Lamin A/C Null Mice [ChIP-Seq]

(Submitter supplied) Deletion of Lmna, encoding nuclear membrane protein LMNA, specifically in mouse cardiac myocytes activates BRD4 and leads to heart failure, arrhythmias, myocardial fibrosis, apoptosis, and premature death, which were partially rescued upon inhibition of BRD4.

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL21493
16 Samples

Download data: BED

Series

Accession:: GSE142127

ID:: 200142127

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Select item 2001239164.

TP53/DNA Damage Response Pathway is Activated and Contributes to the Pathogenesis of Dilated Cardiomyopathy Caused by Lamin A/C Mutations

(Submitter supplied) To gain insights into the molecular pathogenesis of DCM caused by LMNA mutation, a doxycycline-inducible (Dox-Off) gene expression system was used to express either a wild type (WT) or a mutant LMNA containing the pathogenic variant p.Asp300Asn (LMNAD300N) in cardiac myocytes. The LMNAD300N is associated with DCM in patients with atypical progeroid/Werner syndrome and non-syndromic cardiac progeria. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL21103
8 Samples

Download data: TXT

Series

Accession:: GSE123916

ID:: 200123916

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Select item 2001520055.

BET Bromodomain Proteins Regulate Transcriptional Reprogramming in Genetic Dilated Cardiomyopathy

(Submitter supplied) In a model of chronic heart failure, BET bromodomain inhibition delayed cardiac remodeling and fibrosis by halting pathologic inflammatory gene networks in an NFkB-dependent manner.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL19057
48 Samples

Download data: TXT

Series

Accession:: GSE152005

ID:: 200152005

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Select item 2001336936.

Myocardial RNA Sequence Analyses throughout the Course of Mouse Cardiac Laminopathy Identify Differential Expressions of the Key Genes for Cell Cycle Control and Mitochondrial Function

(Submitter supplied) Gene expression profiling in homozygous LMNA-/- mouse model with cardiomyopathy phenotype unraveled novel LMNA-mediated alterations of signaling pathways leading to dilated cardiomyopathy

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL17021
18 Samples

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Series

Accession:: GSE133693

ID:: 200133693

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Select item 2001909777.

TEAD1 trapping by the Q353R-Lamin A/C causes dilated cardiomyopathy.

(Submitter supplied) • Mutations in the LMNA gene encoding Lamin A and C (Lamin A/C), major components of the nuclear lamina, cause laminopathies including dilated cardiomyopathy (DCM), but the underlying molecular mechanisms have not been fully elucidated. Here, by leveraging single-cell RNA-seq, ATAC-seq, protein array, and electron microscopy analysis, we show that insufficient structural maturation of cardiomyocytes owing to trapping of transcription factor TEAD1 by mutant Lamin A/C at the nuclear membrane underlies the pathogenesis of Q353R- LMNA-related DCM. more...

Organism:: Homo sapiens; Mus musculus

Type:: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL16791 GPL24247 GPL24676
30 Samples

Download data: BW, CSV, H5, MTX, TSV

Series

Accession:: GSE190977

ID:: 200190977

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Select item 2001103418.

RNA-seq of control and Lmna -/- mice heart samples

(Submitter supplied) RNA-sequencing analysis from whole heart ribosome depleted RNA from the 2-week old WT and Lmna-/- mice (N=5) . Strand specific RNA seq libraries where prepared form ribosome-depleted cardiac RNA samples using the Illumina TruSeq stranded total RNA library preparation kit. The samples weresequenced on the Illumina HiSeq 4000 instrument using the paired-end sequencing reagents to generate100 base paired end reads.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL21103
10 Samples

Download data: XLSX

Series

Accession:: GSE110341

ID:: 200110341

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Select item 2001208389.

Genomic Reorganization of Lamin-Associated Domains in Cardiac Myocytes is Associated with Differential Gene Expression and DNA Methylation in Human Dilated Cardiomyopathy

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL21290 GPL20301
30 Samples

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Series

Accession:: GSE120838

ID:: 200120838

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Select item 20012083710.

Genomic Reorganization of Lamin-Associated Domains in Cardiac Myocytes is Associated with Differential Gene Expression and DNA Methylation in Human Dilated Cardiomyopathy [ChIP-Seq]

(Submitter supplied) Mutations in the LMNA gene causes set of disorders collectively referred to as laminopathies that include dilated cardiomyopathy. Lamin A/C proteins a components of nuclear lamina forms distinct nuclear domains called lamina associated domains (LADs). The roles of LADs in DCM is not known. To identify LADs and characterize their associations with CpG methylation and gene expression in human cardiac myocytes isolated from patients with DCM and controls we performed Chromatin immunoprecipitation-sequencing (ChIP-Seq), reduced representative bisulfite sequencing (RRBS), and RNA-sequencing (RNA-Seq) in 5 control and 5 DCM hearts with defined pathogenic variants in the LMNA gene. more...

Organism:: Homo sapiens

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL21290
20 Samples

Download data: XLSX

Series

Accession:: GSE120837

ID:: 200120837

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Select item 20012083611.

Genomic Reorganization of Lamin-Associated Domains in Cardiac Myocytes is Associated with Differential Gene Expression and DNA Methylation in Human Dilated Cardiomyopathy [RNA-Seq]

(Submitter supplied) Mutations in the LMNA gene causes set of disorders collectively referred to as laminopathies that include dilated cardiomyopathy. Lamin A/C proteins a components of nuclear lamina forms distinct nuclear domains called lamina associated domains (LADs). The roles of LADs in DCM is not known. To identify LADs and characterize their associations with CpG methylation and gene expression in human cardiac myocytes isolated from patients with DCM and controls we performed Chromatin immunoprecipitation-sequencing (ChIP-Seq), reduced representative bisulfite sequencing (RRBS), and RNA-sequencing (RNA-Seq) in 5 control and 5 DCM hearts with defined pathogenic variants in the LMNA gene. more...

Organism:: Homo sapiens

Type:: Expression profiling by high throughput sequencing

Platform:: GPL20301
10 Samples

Download data: XLSX

Series

Accession:: GSE120836

ID:: 200120836

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Select item 20024159012.

Pervasive nuclear envelope ruptures precede ECM signaling and disease onset without activating cGAS-STING in Lamin-cardiomyopathy mice

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing; Other

Platforms:: GPL24247 GPL17021
163 Samples

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Series

Accession:: GSE241590

ID:: 200241590

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Select item 20024158913.

Pervasive nuclear envelope ruptures precede ECM signaling and disease onset without activating cGAS-STING in Lamin cardiomyopathy mice [SLAM-IT-seq]

(Submitter supplied) Nuclear envelope (NE) ruptures are emerging observations in Lamin-related dilated cardiomyopathy, an adult-onset disease caused by loss-of-function mutations in Lamin A/C, a nuclear lamina component. Here, we test a prevailing hypothesis that NE ruptures trigger the pathological cGAS-STING cytosolic DNA-sensing pathway using a mouse model of Lamin cardiomyopathy. The reduction of Lamin A/C in cardiomyocytes of adult mice causes pervasive NE ruptures in cardiomyocytes, preceding inflammatory transcription, fibrosis, and fatal dilated cardiomyopathy. more...

Organism:: Mus musculus

Type:: Other

Platform:: GPL24247
21 Samples

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Series

Accession:: GSE241589

ID:: 200241589

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Select item 20024158714.

Pervasive nuclear envelope ruptures precede ECM signaling and disease onset without activating cGAS-STING in Lamin cardiomyopathy mice [sci-RNA-seq]

(Submitter supplied) Nuclear envelope (NE) ruptures are emerging observations in Lamin-related dilated cardiomyopathy, an adult-onset disease caused by loss-of-function mutations in Lamin A/C, a nuclear lamina component. Here, we test a prevailing hypothesis that NE ruptures trigger the pathological cGAS-STING cytosolic DNA-sensing pathway using a mouse model of Lamin cardiomyopathy. The reduction of Lamin A/C in cardiomyocytes of adult mice causes pervasive NE ruptures in cardiomyocytes, preceding inflammatory transcription, fibrosis, and fatal dilated cardiomyopathy. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL24247
96 Samples

Download data: CSV, RDS

Series

Accession:: GSE241587

ID:: 200241587

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Select item 20024157715.

Pervasive nuclear envelope ruptures precede ECM signaling and disease onset without activating cGAS-STING in Lamin-cardiomyopathy mice [mRNA-seq]

(Submitter supplied) Nuclear envelope (NE) ruptures are emerging observations in Lamin-related dilated cardiomyopathy, an adult-onset disease caused by loss-of-function mutations in Lamin A/C, a nuclear lamina component. Here, we test a prevailing hypothesis that NE ruptures trigger the pathological cGAS-STING cytosolic DNA-sensing pathway using a mouse model of Lamin cardiomyopathy. The reduction of Lamin A/C in cardiomyocytes of adult mice causes pervasive NE ruptures in cardiomyocytes, preceding inflammatory transcription, fibrosis, and fatal dilated cardiomyopathy. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platforms:: GPL17021 GPL24247
46 Samples

Download data: CSV

Series

Accession:: GSE241577

ID:: 200241577

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Select item 20012926516.

Dynamic chromatin targeting of BRD4 stimulates cardiac fibroblast activation [RNA-seq_Mm]

(Submitter supplied) Small molecule inhibitors of the acetyl-histone binding protein BRD4 have been shown to block cardiac fibrosis in pre-clinical models of heart failure (HF). However, the mechanisms by which BRD4 promotes pathological myocardial fibrosis remain unclear. Here, we demonstrate that BRD4 functions as an effector of TGF-b signaling to stimulate conversion of quiescent cardiac fibroblasts into Periostin (Postn)-positive cells that express high levels of extracellular matrix. more...

Organism:: Mus musculus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL21103
10 Samples

Download data: TXT, XLS

Series

Accession:: GSE129265

ID:: 200129265

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Select item 20012723017.

Dynamic chromatin targeting of BRD4 stimulates cardiac fibroblast activation

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:: Mus musculus; Rattus norvegicus

Type:: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing

Platforms:: GPL14844 GPL18694 GPL21103
25 Samples

Download data: BED, WIG

Series

Accession:: GSE127230

ID:: 200127230

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Select item 20012722918.

Dynamic chromatin targeting of BRD4 stimulates cardiac fibroblast activation [RNA-seq]

(Submitter supplied) Small molecule inhibitors of the acetyl-histone binding protein BRD4 have been shown to block cardiac fibrosis in pre-clinical models of heart failure (HF). However, the mechanisms by which BRD4 promotes pathological myocardial fibrosis remain unclear. Here, we demonstrate that BRD4 functions as an effector of TGF-b signaling to stimulate conversion of quiescent cardiac fibroblasts into Periostin (Postn)-positive cells that express high levels of extracellular matrix. more...

Organism:: Rattus norvegicus

Type:: Expression profiling by high throughput sequencing

Platform:: GPL18694
9 Samples

Download data: TXT

Series

Accession:: GSE127229

ID:: 200127229

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20012721419.

Dynamic chromatin targeting of BRD4 stimulates cardiac fibroblast activation [ChIP-seq]

(Submitter supplied) Small molecule inhibitors of the acetyl-histone binding protein BRD4 have been shown to block cardiac fibrosis in pre-clinical models of heart failure (HF). However, the mechanisms by which BRD4 promotes pathological myocardial fibrosis remain unclear. Here, we demonstrate that BRD4 functions as an effector of TGF-b signaling to stimulate conversion of quiescent cardiac fibroblasts into Periostin (Postn)-positive cells that express high levels of extracellular matrix. more...