DNA Damage Response/TP53 Pathway Is Activated and Contributes to the Pathogenesis of Dilated Cardiomyopathy Associated With LMNA (Lamin A/C) Mutations.
cardiomyopathies
heart failure
humans
mice
transcriptome
Journal
Circulation research
ISSN: 1524-4571
Titre abrégé: Circ Res
Pays: United States
ID NLM: 0047103
Informations de publication
Date de publication:
15 03 2019
15 03 2019
Historique:
pubmed:
31
1
2019
medline:
31
12
2019
entrez:
31
1
2019
Statut:
ppublish
Résumé
Mutations in the LMNA gene, encoding LMNA (lamin A/C), are responsible for laminopathies. Dilated cardiomyopathy (DCM) is a major cause of mortality and morbidity in laminopathies. To gain insights into the molecular pathogenesis of DCM in laminopathies. We generated a tet-off bigenic mice expressing either a WT (wild type) or a mutant LMNA (D300N) protein in cardiac myocytes. LMNA Cardiac myocyte-specific expression of LMNA
Identifiants
pubmed: 30696354
doi: 10.1161/CIRCRESAHA.118.314238
pmc: PMC6460911
mid: NIHMS1519967
doi:
Substances chimiques
E2F Transcription Factors
0
Lamin Type A
0
Lmna protein, mouse
0
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
856-873Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL088498
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL132401
Pays : United States
Organisme : NIH HHS
ID : S10 OD018135
Pays : United States
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