ArticleMolecular and cellular biology1997
Signaling through mitogen-activated protein kinase and Rac/Rho does not duplicate the effects of activated Ras on skeletal myogenesis.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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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Who cites it
24 citing papers in PubMed, 80 citations in OpenAlex.
- Grb2/Sos1 signaling regulates the number of reserve cells in C2C12 cell culture.In vitro cellular & developmental biology. Animal · 2026Article
- M-Ras induces Ral and JNK activation to regulate MEK/ERK-independent gene expression in MCF-7 breast cancer cells.Journal of cellular biochemistry · 2012Article
- The myogenic kinome: protein kinases critical to mammalian skeletal myogenesis.Skeletal muscle · 2011Article
- Neurofibromin (Nf1) is required for skeletal muscle development.Human molecular genetics · 2011Article
- Batf promotes growth arrest and terminal differentiation of mouse myeloid leukemia cells.Molecular cancer research : MCR · 2011Article
- Cardiotrophin-1 maintains the undifferentiated state in skeletal myoblasts.The Journal of biological chemistry · 2009Article
- Article
- Rb and N-ras function together to control differentiation in the mouse.Molecular and cellular biology · 2003Article
- EBNA2 and activated Notch induce expression of BATF.Journal of virology · 2003Article
- Alteration of mesodermal cell differentiation by EWS/FLI-1, the oncogene implicated in Ewing's sarcoma.Molecular and cellular biology · 2003Article
- Article
- A protein kinase B-dependent and rapamycin-sensitive pathway controls skeletal muscle growth but not fiber type specification.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Role of SHP-2 in fibroblast growth factor receptor-mediated suppression of myogenesis in C2C12 myoblasts.Molecular and cellular biology · 2002Article
- Atypical protein kinase Cs are the Ras effectors that mediate repression of myogenic satellite cell differentiation.Molecular and cellular biology · 2002Article
- Article
- Critical activities of Rac1 and Cdc42Hs in skeletal myogenesis: antagonistic effects of JNK and p38 pathways.Molecular biology of the cell · 2000Article
- B-ATF functions as a negative regulator of AP-1 mediated transcription and blocks cellular transformation by Ras and Fos.Oncogene · 2000Article
- Positive regulation of skeletal myogenesis by R-Ras.Oncogene · 2000Article
- Ras signaling through PI3K confers hormone-independent proliferation that is compatible with differentiation.Oncogene · 2000Article
- The retinoblastoma protein is linked to the activation of Ras.Molecular and cellular biology · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The ability of basic helix-loop-helix muscle regulatory factors (MRFs), such as MyoD, to convert nonmuscle cells to a myogenic lineage is regulated by numerous growth factor and oncoprotein signaling pathways. Previous studies have shown that H-Ras 12V inhibits differentiation to a skeletal muscle lineage by disrupting MRF function via a mechanism that is independent of the dimerization, DNA binding, and inherent transcriptional activation properties of the proteins. To investigate the intracellular signaling pathway(s) that mediates the inhibition of MRF-induced myogenesis by oncogenic Ras, we tested two transformation-defective H-Ras 12V effector domain variants for their ability to alter terminal differentiation. H-Ras 12V,35S retains the ability to activate the Raf/MEK/mitogen-activated protein (MAP) kinase cascade, whereas H-Ras 12V,40C is unable to interact directly with Raf-1 yet still influences other signaling intermediates, including Rac and Rho. Expression of each H-Ras 12V variant in C3H10T1/2 cells abrogates MyoD-induced activation of the complete myogenic program, suggesting that MAP kinase-dependent and -independent Ras signaling pathways individually block myogenesis in this model system. However, additional studies with constitutively activated Rac1 and RhoA proteins revealed no negative effects on MyoD-induced myogenesis. Similarly, treatment of Ras-inhibited myoblasts with the MEK1 inhibitor PD98059 revealed that elevated MAP kinase activity is not a significant contributor to the H-Ras 12V effect. These data suggest that an additional Ras pathway, distinct from the well-characterized MAP kinase and Rac/Rho pathways known to be important for the transforming function of activated Ras, is primarily responsible for the inhibition of myogenesis by H-Ras 12V.
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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.