ArticleOncogene2008
Delineating v-Src downstream effector pathways in transformed myoblasts.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 16 citations in OpenAlex.
- Testing calpain inhibition in tumor endothelial cells: novel targetable biomarkers against glioblastoma malignancy.Frontiers in oncology · 2024Article
- Phase I and pharmacokinetics/pharmacodynamics study of the MEK inhibitor RO4987655 in Japanese patients with advanced solid tumors.Investigational new drugs · 2015Article
- Temporal analysis of reciprocal miRNA-mRNA expression patterns predicts regulatory networks during differentiation in human skeletal muscle cells.Physiological genomics · 2015Article
- The role of Na+/K+-ATPase during chick skeletal myogenesis.PloS one · 2015Article
- A cardiac-enriched microRNA, miR-378, blocks cardiac hypertrophy by targeting Ras signaling.The Journal of biological chemistry · 2013Article
- Article
- Calpains as potential anti-cancer targets.Expert opinion on therapeutic targets · 2011Review
- MicroRNAs in skeletal myogenesis.Cell cycle (Georgetown, Tex.) · 2011Review
- Identification of c-Src tyrosine kinase substrates in platelet-derived growth factor receptor signaling.Molecular oncology · 2009Article
- Microrna-221 and microrna-222 modulate differentiation and maturation of skeletal muscle cells.PloS one · 2009Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we delineate the intracellular signalling pathways modulated by a conditional v-Src tyrosine kinase that lead to unrestrained proliferation and block of differentiation of primary avian myoblasts. By inhibiting Ras-MAPK kinase and phosphatidylinositol 3-kinase with different means, we find that both pathways play crucial roles in controlling v-Src-sustained growth factor and anchorage independence for proliferation. The Ras-MAPK kinase pathway also contributes to block of differentiation independently of cell proliferation since inhibition of this pathway both in proliferating and growth-arrested v-Src-transformed myoblasts induces expression of muscle-specific genes, fusion into multinucleated myotubes and assembly of specialized contractile structures. Importantly, we find that the p38 MAPK pathway is inhibited by v-Src in myoblasts and its forced activation results in growth inhibition and expression of differentiation, indicating p38 MAPK as a critical target of v-Src in growth transformation and myogenic differentiation. Furthermore, we show that downregulation of p38 MAPK activation may occur via Ras-MAPK kinase, thus highlighting a cross-regulation between the two pathways. Finally, we report that the simultaneous inhibition of MAPK kinase and calpain, combined to activation of p38 MAPK, are sufficient to reconstitute largely the differentiation potential of v-Src-transformed myoblasts.
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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.