ArticleOncogene2000
No requirement for src family kinases for PDGF signaling in fibroblasts expressing SV40 large T antigen.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 45 citations in OpenAlex.
- SRC IncreasesMolecular and cellular biology · 2018Article
- Oncogenic Ras/Src cooperativity in pancreatic neoplasia.Oncogene · 2011Article
- MicroRNA control of podosome formation in vascular smooth muscle cells in vivo and in vitro.The Journal of cell biology · 2010Article
- The Csk-binding protein PAG regulates PDGF-induced Src mitogenic signaling via GM1.The Journal of cell biology · 2008Article
- The adaptor protein Tom1L1 is a negative regulator of Src mitogenic signaling induced by growth factors.Molecular and cellular biology · 2006Article
- Divergent roles of c-Src in controlling platelet-derived growth factor-dependent signaling in fibroblasts.Molecular biology of the cell · 2005Article
- Absence of Fyn and Src causes a reeler-like phenotype.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Role of Stat3 in regulating p53 expression and function.Molecular and cellular biology · 2005Article
- Malignant transformation but not normal cell growth depends on signal transducer and activator of transcription 3.Cancer research · 2005Article
- Review
- RACK1 regulates G1/S progression by suppressing Src kinase activity.Molecular and cellular biology · 2004Article
- The role of protein tyrosine phosphatase 1B in Ras signaling.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- c-Abl is an effector of Src for growth factor-induced c-myc expression and DNA synthesis.The EMBO journal · 2002Article
- v-Src-induced modulation of the calpain-calpastatin proteolytic system regulates transformation.Molecular and cellular biology · 2002Article
- Stat3-mediated Myc expression is required for Src transformation and PDGF-induced mitogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Natural biology of polyomavirus middle T antigen.Microbiology and molecular biology reviews : MMBR · 2001Review
- SU6656, a selective src family kinase inhibitor, used to probe growth factor signaling.Molecular and cellular biology · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing body of literature suggests that the ubiquitously expressed Src family kinases (Src, Fyn and Yes) are required for agents such as platelet-derived growth factor (PDGF) to stimulate DNA synthesis. Yet Klinghoffer and colleagues recently presented evidence that fibroblasts derived from mice null for Src, Fyn and Yes responded normally to PDGF (Klinghoffer et al., 1999, EMBO J., 18: 2459 - 2471). What is the reason for this discrepancy? We noted that Klinghoffer et al. (1999) used SV40 large T antigen (largeT) to facilitate derivation of cell lines from the embryos. We therefore tested the effect of largeT on PDGF receptor signaling. We found that expression of largeT overcame the inhibitory effects of interfering forms of both Ras (N17Ras) and Src (SrcK-). Furthermore, injection of SrcK- or the cst.1 antibody (which inhibits Src, Fyn and Yes) failed to inhibit PDGF-stimulated DNA synthesis in NIH3T3 cells expressing dominant negative p53, and fibroblasts derived from p53 null embryos. These data suggest firstly that caution should be used in interpretation of experiments conducted in cell lines expressing largeT, and secondly that the role of Src family kinases in growth factor signaling may be to oppose the effects of negative growth regulators such as p53. Oncogene (2000) 19, 2867 - 2869
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