ArticleCirculation research2012
CIP, a cardiac Isl1-interacting protein, represses cardiomyocyte hypertrophy.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Treatment with the Nox1/4 inhibitor Setanaxib ameliorates cardiac function in mouse models of Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Review
- The effects of β-catenin on cardiomyogenesis via Islet-1 and MLIP ubiquitination.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Novel homozygous nonsense mutation of MLIP and compensatory alternative splicing.NPJ genomic medicine · 2022Article
- MicroRNA-130a attenuates cardiac fibrosis after myocardial infarction through TGF-β/Smad signaling by directly targeting TGF-β receptor 1.Bioengineered · 2022Article
- Cardiac CIP protein regulates dystrophic cardiomyopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Cardiac ISL1-Interacting Protein, a Cardioprotective Factor, Inhibits the Transition From Cardiac Hypertrophy to Heart Failure.Frontiers in cardiovascular medicine · 2022Article
- Loss of mFrontiers in cardiovascular medicine · 2022Article
- The cardiac translational landscape reveals that micropeptides are new players involved in cardiomyocyte hypertrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Muscle Enriched Lamin Interacting Protein (Cells · 2021Article
- Spotlight on Isl1: A Key Player in Cardiovascular Development and Diseases.Frontiers in cell and developmental biology · 2021Review
- Intercalated disc protein Xinβ is required for Hippo-YAP signaling in the heart.Nature communications · 2020Article
- Regulation of myonuclear positioning and muscle function by the skeletal muscle-specific CIP protein.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Expression of murine muscle-enriched A-type lamin-interacting protein (MLIP) is regulated by tissue-specific alternative transcription start sites.The Journal of biological chemistry · 2018Article
- How cardiomyocytes sense pathophysiological stresses for cardiac remodeling.Cellular and molecular life sciences : CMLS · 2017Review
- Exome-wide association study reveals novel susceptibility genes to sporadic dilated cardiomyopathy.PloS one · 2017Article
- MicroRNA-155 facilitates skeletal muscle regeneration by balancing pro- and anti-inflammatory macrophages.Cell death & disease · 2016Article
- Cardiomyocyte-enriched protein CIP protects against pathophysiological stresses and regulates cardiac homeostasis.The Journal of clinical investigation · 2015Article
- 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.The Journal of biological chemistry · 2015Article
- Wnt-promoted Isl1 expression through a novel TCF/LEF1 binding site and H3K9 acetylation in early stages of cardiomyocyte differentiation of P19CL6 cells.Molecular and cellular biochemistry · 2014Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleMammalian heart has minimal regenerative capacity. In response to mechanical or pathological stress, the heart undergoes cardiac remodeling. Pressure and volume overload in the heart cause increased size (hypertrophic growth) of cardiomyocytes. Whereas the regulatory pathways that activate cardiac hypertrophy have been well-established, the molecular events that inhibit or repress cardiac hypertrophy are less known.
objectiveTo identify and investigate novel regulators that modulate cardiac hypertrophy. METHODS AND
resultsHere, we report the identification, characterization, and functional examination of a novel cardiac Isl1-interacting protein (CIP). CIP was identified from a bioinformatic search for novel cardiac-expressed genes in mouse embryonic hearts. CIP encodes a nuclear protein without recognizable motifs. Northern blotting, in situ hybridization, and reporter gene tracing demonstrated that CIP is highly expressed in cardiomyocytes of developing and adult hearts. Yeast two-hybrid screening identified Isl1, a LIM/homeodomain transcription factor essential for the specification of cardiac progenitor cells in the second heart field, as a cofactor of CIP. CIP directly interacted with Isl1, and we mapped the domains of these two proteins, which mediate their interaction. We show that CIP represses the transcriptional activity of Isl1 in the activation of the myocyte enhancer factor 2C. The expression of CIP was dramatically reduced in hypertrophic cardiomyocytes. Most importantly, overexpression of CIP repressed agonist-induced cardiomyocyte hypertrophy.
conclusionsOur studies therefore identify CIP as a novel regulator of cardiac hypertrophy.
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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 OpenQuestion graph.