ArticleCell death and differentiation2012
The histone- and PRMT5-associated protein COPR5 is required for myogenic differentiation.
Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- Exploring structural diversity and dynamic stability of small-molecule PRMT5 inhibitors through machine learning-based QSAR and molecular modelling.Molecular diversity · 2026Article
- The negative adipogenesis regulatoreLife · 2023Article
- PRMT5 links lipid metabolism to contractile function of skeletal muscles.EMBO reports · 2023Article
- Inhibition of histone methyltransferase PRMT5 attenuates cisplatin-induced hearing loss through the PI3K/Akt-mediated mitochondrial apoptotic pathway.Journal of pharmaceutical analysis · 2023Article
- Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022Review
- Discovery and Biological Characterization of PRMT5:MEP50 Protein-Protein Interaction Inhibitors.Journal of medicinal chemistry · 2022Article
- Endothelial PRMT5 plays a crucial role in angiogenesis after acute ischemic injury.JCI insight · 2022Article
- The uncharacterized protein FAM47E interacts with PRMT5 and regulates its functions.Life science alliance · 2021Article
- Role of Protein Arginine Methyltransferases and Inflammation in Muscle Pathophysiology.Frontiers in physiology · 2021Review
- MLL1 promotes myogenesis by epigenetically regulating Myf5.Cell proliferation · 2020Article
- PRMT5 Cooperates with pICln to Function as a Master Epigenetic Activator of DNA Double-Strand Break Repair Genes.iScience · 2020Article
- NF1 microdeletion syndrome: case report of two new patients.Italian journal of pediatrics · 2019Article
- Protein arginine methyltransferase expression and activity during myogenesis.Bioscience reports · 2018Article
- Temporal regulation of chromatin during myoblast differentiation.Seminars in cell & developmental biology · 2017Review
- Emerging genotype-phenotype relationships in patients with large NF1 deletions.Human genetics · 2017Review
- Regulation of Skeletal Muscle Plasticity by Protein Arginine Methyltransferases and Their Potential Roles in Neuromuscular Disorders.Frontiers in physiology · 2017Review
- Promoter-enhancer looping at the PPARγ2 locus during adipogenic differentiation requires the Prmt5 methyltransferase.Nucleic acids research · 2016Article
- The PRMT5 arginine methyltransferase: many roles in development, cancer and beyond.Cellular and molecular life sciences : CMLS · 2015Review
- The Wnt-target gene Dlk-1 is regulated by the Prmt5-associated factor Copr5 during adipogenic conversion.Biology open · 2015Article
- miR-24 affects hair follicle morphogenesis targeting Tcf-3.Cell death & disease · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myogenic differentiation requires the coordination between permanent cell cycle withdrawal, mediated by members of the cyclin-dependent kinase inhibitor (CKI) family, and activation of a cascade of myogenic transcription factors, particularly MYOGENIN (MYOG). Recently, it has been reported that the Protein aRginine Methyl Transferase PRMT5 modulates the early phase of induction of MYOG expression. Here, we show that the histone- and PRMT5-associated protein COPR5 (cooperator of PRMT5) is required for myogenic differentiation. C2C12 cells, in which COPR5 had been silenced, could not irreversibly exit the cell cycle and differentiate into muscle cells. This phenotype might be explained by the finding that, in cells in which COPR5 was downregulated, p21 and MYOG induction was strongly reduced and PRMT5 recruitment to the promoters of these genes was also altered. Moreover, we suggest that COPR5 interaction with the Runt-related transcription factor 1 (RUNX1)-core binding factor-β (CBFβ) complex contributes to targeting the COPR5-PRMT5 complex to these promoters. Finally, we present evidence that COPR5 depletion delayed the in vivo regeneration of cardiotoxin-injured mouse skeletal muscles. Altogether, these data extend the role of COPR5 from an adaptor protein required for nuclear functions of PRMT5 to an essential coordinator of myogenic differentiation.
Indexed as
Identifiers
What OpenQuestion holds
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.