ArticlePloS one2016
Cdo Regulates Surface Expression of Kir2.1 K+ Channel in Myoblast Differentiation.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
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- Endothelial PRMT7 prevents dysfunction, promotes revascularization and enhances cardiac recovery post-myocardial infarction.Experimental & molecular medicine · 2025Article
- Advancements in the study of inward rectifying potassium channels on vascular cells.Channels (Austin, Tex.) · 2023Review
- PRMT7 ablation in cardiomyocytes causes cardiac hypertrophy and fibrosis through β-catenin dysregulation.Cellular and molecular life sciences : CMLS · 2022Article
- Slight up-regulation of Kir2.1 channel promotes endothelial progenitor cells to transdifferentiate into a pericyte phenotype by Akt/mTOR/Snail pathway.Journal of cellular and molecular medicine · 2021Article
- Oscillating shear stress mediates mesenchymal transdifferentiation of EPCs by the Kir2.1 channel.Heart and vessels · 2020Article
- Satellite cell-specific ablation of Cdon impairs integrin activation, FGF signalling, and muscle regeneration.Journal of cachexia, sarcopenia and muscle · 2020Article
- Article
- Prmt7 promotes myoblast differentiation via methylation of p38MAPK on arginine residue 70.Cell death and differentiation · 2020Article
- The LRRC8/VRAC anion channel facilitates myogenic differentiation of murine myoblasts by promoting membrane hyperpolarization.The Journal of biological chemistry · 2019Article
- Ginsenoside Rg1 augments oxidative metabolism and anabolic response of skeletal muscle in mice.Journal of ginseng research · 2019Article
- Skeletal muscle-specific Prmt1 deletion causes muscle atrophy via deregulation of the PRMT6-FOXO3 axis.Autophagy · 2019Article
- Bioelectric Properties of Myogenic Progenitor Cells.Bioelectricity · 2019Review
- IGDB-2, an Ig/FNIII protein, binds the ion channel LGC-34 and controls sensory compartment morphogenesis in C. elegans.Developmental biology · 2017Article
- Keep Your Friends Close: Cell-Cell Contact and Skeletal Myogenesis.Cold Spring Harbor perspectives in biology · 2017Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A potassium channel Kir2.1-associated membrane hyperpolarization is required for myogenic differentiation. However the molecular regulatory mechanisms modulating Kir2.1 channel activities in early stage of myogenesis are largely unknown. A cell surface protein, Cdo functions as a component of multiprotein cell surface complexes to promote myogenesis. In this study, we report that Cdo forms a complex with Kir2.1 during myogenic differentiation, and is required for the channel activity by enhancing the surface expression of Kir2.1 in the early stage of differentiation. The expression of a constitutively active form of the upstream kinase for p38MAPK, MKK6(EE) can restore Kir2.1 activities in Cdo-depleted C2C12 cells, while the treatment with a p38MAPK inhibitor, SB203580 exhibits a similar effect of Cdo depletion on Kir2.1 surface expression. Furthermore, Cdo-/- primary myoblasts, which display a defective differentiation program, exhibit a defective Kir2.1 activity. Taken together, our results suggest that a promyogenic Cdo signaling is critical for Kir2.1 activities in the induction of myogenic differentiation.
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