ArticleMolecular and cellular biology1996
Cyclin-mediated inhibition of muscle gene expression via a mechanism that is independent of pRB hyperphosphorylation.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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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Who cites it
60 citing papers in PubMed, 134 citations in OpenAlex.
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- Exon skipping in genes encoding lineage-defining myogenic transcription factors in rhabdomyosarcoma.Cold Spring Harbor molecular case studies · 2022Article
- Key Genes Regulating Skeletal Muscle Development and Growth in Farm Animals.Animals : an open access journal from MDPI · 2021Review
- Epigenetic regulation of satellite cell fate during skeletal muscle regeneration.Skeletal muscle · 2021Review
- Kinetin stimulates differentiation of C2C12 myoblasts.PloS one · 2021Article
- Beyond What Your Retina Can See: Similarities of Retinoblastoma Function between Plants and Animals, from Developmental Processes to Epigenetic Regulation.International journal of molecular sciences · 2020Review
- YY1 regulates skeletal muscle regeneration through controlling metabolic reprogramming of satellite cells.The EMBO journal · 2019Article
- Low-level laser irradiation induces a transcriptional myotube-like profile in C2C12 myoblasts.Lasers in medical science · 2018Article
- Genome-Wide Association Analysis With a 50K Transcribed Gene SNP-Chip Identifies QTL Affecting Muscle Yield in Rainbow Trout.Frontiers in genetics · 2018Article
- Stomagenesis versus myogenesis: Parallels in intrinsic and extrinsic regulation of transcription factor mediated specialized cell-type differentiation in plants and animals.Development, growth & differentiation · 2016Review
- Non-canonical functions of cell cycle cyclins and cyclin-dependent kinases.Nature reviews. Molecular cell biology · 2016Review
- Negative regulation of initial steps in skeletal myogenesis by mTOR and other kinases.Scientific reports · 2016Article
- Cell Differentiation and Checkpoint.International journal of cancer research and molecular mechanisms · 2015Article
- Brahma is required for cell cycle arrest and late muscle gene expression during skeletal myogenesis.EMBO reports · 2015Article
- Retinoblastoma protein and MyoD function together to effect the repression of Fra-1 and in turn cyclin D1 during terminal cell cycle arrest associated with myogenesis.The Journal of biological chemistry · 2014Article
- Cyclin D3 critically regulates the balance between self-renewal and differentiation in skeletal muscle stem cells.Stem cells (Dayton, Ohio) · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
It was recently demonstrated that ectopic expression of cyclin D1 inhibits skeletal muscle differentiation and, conversely, that expression of cyclin-dependent kinase (cdk) inhibitors facilitates activation of this differentiation program (S. S. Rao, C. Chu, and D. S. Kohtz, Mol. Cell. Biol. 14:5259-5267, 1994; S. S. Rao and D. S. Kohtz, J. Biol. Chem. 270:4093-4100, 1995; S. X. Skapek, J. Rhee, D. B. Spicer, and A. B. Lassar, Science 267:1022-1024, 1995). Here we demonstrate that cyclin D1 inhibits muscle gene expression without affecting MyoD DNA binding activity. Ectopic expression of cyclin D1 inhibits muscle gene activation by both MyoD and myogenin, including a mutated form of myogenin in which two potential inhibitory cdk phosphorylation sites are absent. Because the retinoblastoma gene product, pRB, is a known target for cyclin D1-cdk phosphorylation, we determined whether cyclin D1-mediated inhibition of myogenesis was due to hyperphosphorylation of pRB. In pRB-deficient fibroblasts, the ability of MyoD to activate the expression of muscle-specific genes requires coexpression of ectopic pRB (B. G. Novitch, G. J. Mulligan, T. Jacks, and A. B. Lassar, J. Cell Biol., 135:441-456, 1996). In these cells, the expression of cyclins A and E can lead to pRB hyperphosphorylation and can inhibit muscle gene expression. The negative effects of cyclins A or E on muscle gene expression are, however, reversed by the presence of a mutated form of pRB which cannot be hyperphosphorylated. In contrast, cyclin D1 can inhibit muscle gene expression in the presence of the nonhyperphosphorylatable form of pRB. On the basis of these results we propose that G1 cyclin-cdk activity blocks the initiation of skeletal muscle differentiation by two distinct mechanisms: one that is dependent on pRB hyperphosphorylation and one that is independent of pRB hyperphosphorylation.
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