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This SuperSeries is composed of the following subset Series:; GSE6397: Comparison between gene expression in heart from Lmna H222P heterozygous and control mice; GSE6398: Comparison between gene expression in heart from Lmna H222P homozygous and control mice Experiment Overall Design: Refer to indiv...
ORGANISM(S): Mus musculus 
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 H222...
ORGANISM(S): Mus musculus 
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 H222...
ORGANISM(S): Mus musculus 
Hutchinson-Gilford Progeria Syndrome (HGPS) is caused by a point mutation in the LMNA gene that activates a cryptic donor splice site and yields a truncated form of prelamin A called progerin. Small amounts of progerin are also produced during normal aging. Studies with mouse models of HGPS have all...
ORGANISM(S): Mus musculus 
We performed proteomics analysis on Lmna-/- hearts from mice at 2 weeks and 1 month of age to investigate the underlying mechanism by which LMNA deletion evokes DCM
ORGANISM(S): Mus Musculus 
2023-06-25 | PXD043270 |
ATAC-seq data from Lmna knock-out mouse embryonic fibroblasts (Lmna-/- MEFs) and wild type (Lmna+/+ MEFs)
Alteration of gene expression profile due to Lmna knockout was studied in MEF. Total RNA obtained from Lmna +/+ MEF and Lmna -/- MEF were compared.
ORGANISM(S): Mus musculus 
Over 180 LMNA gene mutations have been identified in human diseases including cardiac and skeletal myopathies, lipodystrophies, and premature aging syndromes. Postulated mechanisms by which these mutations result in different phenotypes include perturbation of normal nuclear structure and chromosom...
ORGANISM(S): Homo sapiens 
Cardiomyocyte-specific lamin A re-expression via AAV-Lmna/DJ8 ameliorates cardiac dysfunction in Lmna⁻/⁻ mice
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