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Inhibition of BRD4 Rescues Cardiac phenotype in Myocyte-Specific Lamin A/C Null Mice

ABSTRACT: Inhibition of BRD4 Rescues Cardiac phenotype in Myocyte-Specific Lamin A/C Null Mice

PROVIDER: PRJNA627374 | ENA |

REPOSITORIES: ENA

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

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

| PRJNA595947 | ENA

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

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

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

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Inhibition of BRD4 Rescues Cardiac phenotype in Myocyte-Specific Lamin A/C Null Mice

Project description: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.

2023-03-19 | GSE149095 | GEO

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

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

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-11-17 | GSE142129 | GEO

Lamin and Lamin B receptor knockout

Project description:influence of lamin B rereceptor knockout and lamin A/C knockout on gene expression in cultured myoblast cells and in striated muscle tissue knockout samples are obtained by mating of heterozygous animals. Homozygous KO and wt animals of one litter are compared. Two boilogical replicates of KO samples are processed in parallel. wt samples are used as controls. One wt sample is processed per KO litter. Where appropriate two wt samples are used as biological replicates.

2013-01-28 | E-GEOD-37076 | biostudies-arrayexpress

Lamin and Lamin B receptor knockout

Project description:influence of lamin B rereceptor knockout and lamin A/C knockout on gene expression in cultured myoblast cells and in striated muscle tissue

2013-01-28 | GSE37076 | GEO

Lamin A/C promotes DNA base excision repair (human arrays)

Project description:The A-type lamins (lamin A/C), encoded by the Lmna gene, are important structural components of the nuclear lamina. Lmna mutations lead to degenerative disorders, including the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). In addition, altered lamin A/C expression is found in various cancers. Reports indicate that lamin A/C plays a role in DNA double strand break repair, but a role in DNA base excision repair (BER) has not been described. We provide evidence for reduced BER efficiency in lamin A/C-depleted cells. The mechanism involves impairment of the APE1 and POLβ enzyme activities in BER. Also, Lmna null mouse fibroblasts displayed reduced expression of several core BER enzymes (PARP1, LIG3, and POLβ). Moreover, the robustness of APE1 and POLβ activities and the rate of BER were enhanced by lamin A/C-augmented poly(ADP-ribose) polymer formation (PARylation). Finally, we report that HGPS fibroblasts are defective in BER. Collectively, our results provide novel insights into the functional interplay between the nuclear lamina and cellular defenses against oxidative DNA damage, with implications for human cancer and aging.

2020-09-30 | GSE124465 | GEO

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