ArticleThe Journal of biological chemistry2015
Deletion of MLIP (muscle-enriched A-type lamin-interacting protein) leads to cardiac hyperactivation of Akt/mammalian target of rapamycin (mTOR) and impaired cardiac adaptation.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Genome-wide association and multi-trait analyses characterize the common genetic architecture of heart failure.Nature communications · 2022Pooled it
- MLIP genotype as a predictor of pharmacological response in primary open-angle glaucoma and ocular hypertension.Scientific reports · 2021Trial
- Nuclear Proteome Map of Mouse Heart Chambers.Molecular & cellular proteomics : MCP · 2026Article
- An integrative single-nucleus multiomic atlas of the human left ventricle identifies gene regulatory network dynamics across cardiac development, aging, and disease.Genome biology · 2026Article
- Mapping DNA methylation to cardiac pathologies induced by beta-adrenergic stimulation in a large panel of mice.Epigenetics · 2025Article
- Large-scale genome-wide association analyses identify novel genetic loci and mechanisms in hypertrophic cardiomyopathy.Nature genetics · 2025Article
- Genome-wide association study reveals mechanisms underlying dilated cardiomyopathy and myocardial resilience.Nature genetics · 2024Article
- Candidate SNP Markers Significantly Altering the Affinity of the TATA-Binding Protein for the Promoters of Human Genes Associated with Primary Open-Angle Glaucoma.International journal of molecular sciences · 2024Article
- Review
- An inflammation resolution-promoting intervention prevents atrial fibrillation caused by left ventricular dysfunction.Cardiovascular research · 2024Article
- MicroRNA205: A Key Regulator of Cardiomyocyte Transition from Proliferative to Hypertrophic Growth in the Neonatal Heart.International journal of molecular sciences · 2024Article
- Native lamin A/C proteomes and novel partners from heart and skeletal muscle in a mouse chronic inflammation model of human frailty.Frontiers in cell and developmental biology · 2023Article
- Genome ofInternational journal of molecular sciences · 2022Article
- Novel homozygous nonsense mutation of MLIP and compensatory alternative splicing.NPJ genomic medicine · 2022Article
- Cardiac CIP protein regulates dystrophic cardiomyopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Neuromuscular disease: 2022 update.Free neuropathology · 2022Article
- Identification of feature genes and pathways for Alzheimer's diseaseFrontiers in computational neuroscience · 2022Article
- MLIP causes recessive myopathy with rhabdomyolysis, myalgia and baseline elevated serum creatine kinase.Brain : a journal of neurology · 2021Article
- Muscle Enriched Lamin Interacting Protein (Cells · 2021Article
- Transcriptomic changes associated with PCK1 overexpression in hepatocellular carcinoma cells detected by RNA-seq.Genes & diseases · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 4 countries.
Funding
Abstract
Aging and diseases generally result from tissue inability to maintain homeostasis through adaptation. The adult heart is particularly vulnerable to disequilibrium in homeostasis because its regenerative abilities are limited. Here, we report that MLIP (muscle enriched A-type lamin-interacting protein), a unique protein of unknown function, is required for proper cardiac adaptation. Mlip(-/-) mice exhibited normal cardiac function despite myocardial metabolic abnormalities and cardiac-specific overactivation of Akt/mTOR pathways. Cardiac-specific MLIP overexpression led to an inhibition of Akt/mTOR, providing evidence of a direct impact of MLIP on these key signaling pathways. Mlip(-/-) hearts showed an impaired capacity to adapt to stress (isoproterenol-induced hypertrophy), likely because of deregulated Akt/mTOR activity. Genome-wide association studies showed a genetic association between Mlip and early response to cardiac stress, supporting the role of MLIP in cardiac adaptation. Together, these results revealed that MLIP is required for normal myocardial adaptation to stress through integrated regulation of the Akt/mTOR pathways.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.