ArticleThe EMBO journal1996
Requirement of phospholipase C gamma, the tyrosine phosphatase Syp and the adaptor proteins Shc and Nck for PDGF-induced DNA synthesis: evidence for the existence of Ras-dependent and Ras-independent pathways.
Article in The EMBO journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 135 citations in OpenAlex.
- Sinner or Saint?: Nck Adaptor Proteins in Vascular Biology.Frontiers in cell and developmental biology · 2021Review
- A patient with germ-line gain-of-function PDGFRB p.N666H mutation and marked clinical response to imatinib.Genetics in medicine : official journal of the American College of Medical Genetics · 2018Article
- Identification of c-Src tyrosine kinase substrates in platelet-derived growth factor receptor signaling.Molecular oncology · 2009Article
- Regulation of process retraction and cell migration by EphA3 is mediated by the adaptor protein Nck1.Biochemistry · 2009Article
- The adaptor protein Tom1L1 is a negative regulator of Src mitogenic signaling induced by growth factors.Molecular and cellular biology · 2006Article
- Kinase activation through dimerization by human SH2-B.Molecular and cellular biology · 2005Article
- Nck-dependent activation of extracellular signal-regulated kinase-1 and regulation of cell survival during endoplasmic reticulum stress.Molecular biology of the cell · 2004Article
- SHP-2 is involved in heterodimer specific loss of phosphorylation of Tyr771 in the PDGF beta-receptor.Oncogene · 2002Article
- c-Abl is an effector of Src for growth factor-induced c-myc expression and DNA synthesis.The EMBO journal · 2002Article
- SU6656, a selective src family kinase inhibitor, used to probe growth factor signaling.Molecular and cellular biology · 2000Article
- Review
- Article
- No requirement for src family kinases for PDGF signaling in fibroblasts expressing SV40 large T antigen.Oncogene · 2000Article
- Slap negatively regulates Src mitogenic function but does not revert Src-induced cell morphology changes.Molecular and cellular biology · 2000Article
- Inositol 1,4,5-trisphosphate directs Ca(2+) flow between mitochondria and the Endoplasmic/Sarcoplasmic reticulum: a role in regulating cardiac autonomic Ca(2+) spiking.Molecular biology of the cell · 2000Article
- Platelet-derived growth factor-dependent association of the GTPase-activating protein of Ras and Src.The Biochemical journal · 1999Article
- Functional Rac-1 and Nck signaling networks are required for FGF-2-induced DNA synthesis in MCF-7 cells.Oncogene · 1999Article
- Cytotoxic T lymphocyte antigen 4 (CTLA-4) engagement delivers an inhibitory signal through the membrane-proximal region in the absence of the tyrosine motif in the cytoplasmic tail.The Journal of experimental medicine · 1999Article
- Physiological requirement for both SH2 domains for phospholipase C-gamma1 function and interaction with platelet-derived growth factor receptors.Molecular and cellular biology · 1999Article
- Article
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
We have investigated the roles of the phosphotyrosine phosphatase Syp (also called SH-PTP2), phospholipase C (PLC) gamma1, rasGTPase Activating Protein (rasGAP) and the adapter molecules Nck and Shc in the mitogenic response induced by PDGF in fibroblasts. Two separate approaches were used to inhibit the biological activity of these signalling proteins in vivo. Either glutathione S-transferase (GST) fusion proteins containing the SH2 domains of these proteins, or antibodies specific for these polypeptides, were microinjected into cells. GST-SH2 fusion proteins are expected to act as dominant inhibitors by competing for physiological SH2-mediated interactions, while microinjected antibodies can directly block protein functions. Inhibition of PLCgamma, Syp, Shc and Nck signals blocked PDGF-stimulated cells in G1 showing a requirement for these proteins for S-phase entry. Inhibition of rasGAP, in contrast, had no effect on S-phase entry. We next examined which of these signals were required for PDGF-induced cFos expression, a Ras-dependent event important for signalling. By using the same approaches with cells expressing beta-galactosidase under the control of a c-fos promoter, we showed that PLCgamma, Syp and Shc were necessary for ligand-induced cFos expression whereas Nck and phosphatidylinositol 3-kinase alpha were not. From these results we concluded that PDGF generates Ras-dependent and Ras-independent pathways important for DNA synthesis.
Indexed as
Identifiers
8890167PMC452231W2227213649What OpenQuestion holds
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.