ArticleCell biochemistry and function2014
Muscle ring finger 1 and muscle ring finger 2 are necessary but functionally redundant during developmental cardiac growth and regulate E2F1-mediated gene expression in vivo.
Article in Cell biochemistry and function, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Exploring TTN variants as genetic insights into cardiomyopathy pathogenesis and potential emerging clues to molecular mechanisms in cardiomyopathies.Scientific reports · 2024Review
- Uncovering the mechanisms of MuRF1-induced ubiquitylation and revealing similarities with MuRF2 and MuRF3.Biochemistry and biophysics reports · 2024Article
- Cardiac sarcomere mechanics in health and disease.Biophysical reviews · 2021Review
- Emerging Strategies Targeting Catabolic Muscle Stress Relief.International journal of molecular sciences · 2020Review
- Article
- Expression of MuRF1 or MuRF2 is essential for the induction of skeletal muscle atrophy and dysfunction in a murine pulmonary hypertension model.Skeletal muscle · 2020Article
- Muscle-specific regulation of right ventricular transcriptional responses to chronic hypoxia-induced hypertrophy by the muscle ring finger-1 (MuRF1) ubiquitin ligase in mice.BMC medical genetics · 2018Article
- Increasing Cardiomyocyte Atrogin-1 Reduces Aging-Associated Fibrosis and Regulates Remodeling in Vivo.The American journal of pathology · 2018Article
- Emergence of Members of TRAF and DUB of Ubiquitin Proteasome System in the Regulation of Hypertrophic Cardiomyopathy.Frontiers in genetics · 2018Review
- The Calcineurin-FoxO-MuRF1 signaling pathway regulates myofibril integrity in cardiomyocytes.eLife · 2017Article
- Cardiac ubiquitin ligases: Their role in cardiac metabolism, autophagy, cardioprotection and therapeutic potential.Biochimica et biophysica acta · 2016Review
- Nebulized Delivery of the MAPKAP Kinase 2 Peptide Inhibitor MMI-0100 Protects Against Ischemia-Induced Systolic Dysfunction.International journal of peptide research and therapeutics · 2016Article
- Cardiomyocyte-Specific Human Bcl2-Associated Anthanogene 3 P209L Expression Induces Mitochondrial Fragmentation, Bcl2-Associated Anthanogene 3 Haploinsufficiency, and Activates p38 Signaling.The American journal of pathology · 2016Article
- MuRF1 mono-ubiquitinates TRα to inhibit T3-induced cardiac hypertrophy in vivo.Journal of molecular endocrinology · 2016Article
- Genome Wide Identification of SARS-CoV Susceptibility Loci Using the Collaborative Cross.PLoS genetics · 2015Article
- MuRF2 regulates PPARγ1 activity to protect against diabetic cardiomyopathy and enhance weight gain induced by a high fat diet.Cardiovascular diabetology · 2015Article
- Muscle ring finger-3 protects against diabetic cardiomyopathy induced by a high fat diet.BMC endocrine disorders · 2015Article
- Non-targeted metabolomics analysis of cardiac Muscle Ring Finger-1 (MuRF1), MuRF2, and MuRF3 in vivo reveals novel and redundant metabolic changes.Metabolomics : Official journal of the Metabolomic Society · 2015Article
- Ongoing controversies surrounding cardiac remodeling: is it black and white-or rather fifty shades of gray?Frontiers in physiology · 2015Review
- The E3 ubiquitin ligase TRIM62 and inflammation-induced skeletal muscle atrophy.Critical care (London, England) · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
aimsMuscle ring finger (MuRF) proteins have been implicated in the transmission of mechanical forces to nuclear cell signaling pathways through their association with the sarcomere. We recently reported that MuRF1, but not MuRF2, regulates pathologic cardiac hypertrophy in vivo. This was surprising given that MuRF1 and MuRF2 interact with each other and many of the same sarcomeric proteins experimentally. METHODS AND
resultsMice missing all four MuRF1 and MuRF2 alleles [MuRF1/MuRF2 double null (DN)] were born with a massive spontaneous hypertrophic cardiomyopathy and heart failure; mice that were null for one of the genes but heterozygous for the other (i.e. MuRF1(-/-) //MuRF2(+/-) or MuRF1(+/-) //MuRF2(-/-) ) were phenotypically identical to wild-type mice. Microarray analysis of genes differentially-expressed between MuRF1/MuRF2 DN, mice missing three of the four alleles and wild-type mice revealed a significant enrichment of genes regulated by the E2F transcription factor family. More than 85% of the differentially-expressed genes had E2F promoter regions (E2f:DP; P<0.001). Western analysis of E2F revealed no differences between MuRF1/MuRF2 DN hearts and wild-type hearts; however, chromatin immunoprecipitation studies revealed that MuRF1/MuRF2 DN hearts had significantly less binding of E2F1 in the promoter regions of genes previously defined to be regulated by E2F1 (p21, Brip1 and PDK4, P<0.01).
conclusionsThese studies suggest that MuRF1 and MuRF2 play a redundant role in regulating developmental physiologic hypertrophy, by regulating E2F transcription factors essential for normal cardiac development by supporting E2F localization to the nucleus, but not through a process that degrades the transcription factor.
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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.