ArticleMolecular and cellular biology2011
Opposing roles of FoxP1 and Nfat3 in transcriptional control of cardiomyocyte hypertrophy.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
24 citing papers in PubMed, 32 citations in OpenAlex.
- Trial
- FoxP1 Represses MEF2A in Striated Muscle.Molecular and cellular biology · 2024Article
- How does NFAT3 regulate the occurrence of cardiac hypertrophy?International journal of cardiology. Heart & vasculature · 2023Review
- Phylogenetic modeling of enhancer shifts in African mole-rats reveals regulatory changes associated with tissue-specific traits.Genome research · 2023Article
- Single-nucleus transcriptomics reveals a gatekeeper role for FOXP1 in primate cardiac aging.Protein & cell · 2023Article
- Targeting the forkhead box protein P1 pathway as a novel therapeutic approach for cardiovascular diseases.Heart failure reviews · 2022Review
- FoxP1 is a transcriptional repressor associated with cancer cachexia that induces skeletal muscle wasting and weakness.Journal of cachexia, sarcopenia and muscle · 2021Article
- The piRNA CHAPIR regulates cardiac hypertrophy by controlling METTL3-dependent NNature cell biology · 2020Article
- NULP1 Alleviates Cardiac Hypertrophy by Suppressing NFAT3 Transcriptional Activity.Journal of the American Heart Association · 2020Article
- Article
- Molecular networks of FOXP family: dual biologic functions, interplay with other molecules and clinical implications in cancer progression.Molecular cancer · 2019Review
- MicroRNAs in Cardiac Diseases.Cells · 2019Review
- Rapid Atrial Pacing Promotes Atrial Fibrillation Substrate in Unanesthetized Instrumented Rats.Frontiers in physiology · 2019Article
- [Mitochondrial aldehyde dehydrogenase 2 protects against high glucose-induced injury in neonatal rat cardiomyocytes by regulating CaN-NFAT3 signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- Visualization of the Genomic Loci That Are Bound by Specific Multiprotein Complexes by Bimolecular Fluorescence Complementation Analysis on Drosophila Polytene Chromosomes.Methods in enzymology · 2017Article
- Developmental SHP2 dysfunction underlies cardiac hypertrophy in Noonan syndrome with multiple lentigines.The Journal of clinical investigation · 2016Article
- In vitro visualization and characterization of wild type and mutant IDH homo- and heterodimers using Bimolecular Fluorescence Complementation.Cancer research frontiers · 2016Article
- miR-206 Mediates YAP-Induced Cardiac Hypertrophy and Survival.Circulation research · 2015Article
- Hippo and Cardiac Hypertrophy: A Complex Interaction.Circulation research · 2015Article
- Visualization of the Drosophila dKeap1-CncC interaction on chromatin illumines cooperative, xenobiotic-specific gene activation.Development (Cambridge, England) · 2014Article
Corrections and comments
- Retraction · 2020-12-21Duplication of/in Image · Manipulation of Images ·
- Retracted
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac homeostasis is maintained by a balance of growth-promoting and growth-modulating factors. Sustained elevation of calcium signaling can induce cardiac hypertrophy through activation of Nfat family transcription factors. FoxP family transcription factors are known to interact with Nfat proteins and to modulate their transcriptional activities in lymphocytes. We investigated FoxP1 interaction with Nfat3 (Nfatc4) and their effects on transcription of hypertrophy-associated genes in neonatal rat cardiomyocytes. FoxP1-Nfat3 complexes were visualized using bimolecular fluorescence complementation (BiFC) analysis. Calcineurin activation induced FoxP1-Nfat3 BiFC complex formation. Amino acid substitutions in the predicted interaction interface inhibited it. FoxP1 repressed hypertrophy-associated genes (Myh7, Rcan1, Cx43, Anf, and Bnp) and counteracted their activation by constitutively nuclear Nfat3 (cnNfat3). In contrast, FoxP1 activated genes that maintain normal heart functions (Myh6 and p57Kip2) and cnNfat3 counteracted their activation by FoxP1. Amino acid substitutions in FoxP1 or cnNfat3 that inhibited their interaction abrogated the activation of hypertrophy-associated gene transcription by cnNfat3 and the repression of these genes by FoxP1. FoxP1 and Nfat3 co-occupied the promoter regions of hypertrophy-associated genes in neonatal and adult heart tissue. FoxP1 counteracted hypertrophic cardiomyocyte growth, and connexin 43 mislocalization caused by cnNfat3 expression. These data suggest that the opposing transcriptional activities of FoxP1 and Nfat3 maintain cardiomyocyte homeostasis.
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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 OpenQuestion graph.