ArticleThe EMBO journal1996
Mutation of a Src phosphorylation site in the PDGF beta-receptor leads to increased PDGF-stimulated chemotaxis but decreased mitogenesis.
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 45 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
45 citing papers in PubMed, 120 citations in OpenAlex.
- Olverembatinib, a novel BCR-ABL tyrosine kinase inhibitor, exhibits anti-tumor activity and synergizes with gemcitabine in pancreatic ductal adenocarcinoma.NPJ precision oncology · 2026Article
- Functional roles of SRC signaling in pancreatic cancer: Recent insights provide novel therapeutic opportunities.Oncogene · 2023Review
- EphA2 signaling within integrin adhesions regulates fibrillar adhesion elongation and fibronectin deposition.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- PDGF-BB enhances collagen gel contraction through a PI3K-PLCγ-PKC-cofilin pathway.Scientific reports · 2017Article
- Article
- PI3 kinase is indispensable for oncogenic transformation by the V560D mutant of c-Kit in a kinase-independent manner.Cellular and molecular life sciences : CMLS · 2015Article
- Ligand-Independent Activation of Platelet-Derived Growth Factor Receptor β during Human Immunodeficiency Virus-Transactivator of Transcription and Cocaine-Mediated Smooth Muscle Hyperplasia.American journal of respiratory cell and molecular biology · 2015Article
- Homo-FRET Based Biosensors and Their Application to Multiplexed Imaging of Signalling Events in Live Cells.International journal of molecular sciences · 2015Article
- Phosphorylation of the activation loop tyrosine 823 in c-Kit is crucial for cell survival and proliferation.The Journal of biological chemistry · 2013Article
- Suppressor of cytokine signaling 2 (SOCS2) associates with FLT3 and negatively regulates downstream signaling.Molecular oncology · 2013Article
- Metazoan-like signaling in a unicellular receptor tyrosine kinase.BMC biochemistry · 2013Article
- Article
- Src, p130Cas, and Mechanotransduction in Cancer Cells.Genes & cancer · 2012Article
- Signaling from the human melanocortin 1 receptor to ERK1 and ERK2 mitogen-activated protein kinases involves transactivation of cKIT.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Identification of c-Src tyrosine kinase substrates in platelet-derived growth factor receptor signaling.Molecular oncology · 2009Article
- Src kinases as therapeutic targets for cancer.Nature reviews. Clinical oncology · 2009Review
- Reciprocal regulation of Abl and receptor tyrosine kinases.Cellular signalling · 2009Article
- The D816V mutation of c-Kit circumvents a requirement for Src family kinases in c-Kit signal transduction.The Journal of biological chemistry · 2009Article
- Growth factors outside of the platelet-derived growth factor (PDGF) family employ reactive oxygen species/Src family kinases to activate PDGF receptor alpha and thereby promote proliferation and survival of cells.The Journal of biological chemistry · 2009Article
- The evolutionarily conserved arrangement of domains in SRC family kinases is important for substrate recognition.Biochemistry · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ligand induced activation of the beta-receptor for platelet-derived growth factor (PDGF) leads to activation of Src family tyrosine kinases. We have explored the possibility that the receptor itself is a substrate for Src. We show that Tyr934 in the kinase domain of the PDGF receptor is phosphorylated by Src. Cell lines expressing a beta-receptor mutant, in which Tyr934 was replaced with a phenyalanine residue, showed reduced mitogenic signaling in response to PDGF-BB. In contrast, the mutant receptor mediated increased signals for chemotaxis and actin reorganization. Whereas the motility responses of cells expressing wild-type beta-receptors were attenuated by inhibition of phosphatidylinositol 3'-kinase, those of cells expressing the mutant receptor were only slightly influenced. In contrast, PDGF-BB-induced chemotaxis of the cells with the mutant receptor was attenuated by inhibition of protein kinase C, whereas the chemotaxis of cells expressing the wild-type beta-receptor was less affected. Moreover, the PDGF-BB-stimulated tyrosine phosphorylation of phospholipase C-gamma was increased in the mutant receptor cells compared with wild-type receptor cells. In conclusion, the characteristics of the Y934F mutant suggest that the phosphorylation of Tyr934 by Src negatively modulates a signal transduction pathway leading to motility responses which involves phospholipase C-gamma, and shifts the response to increased mitogenicity.
Indexed as
Identifiers
8895575PMC452274W1828225209What 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.