ArticleThe EMBO journal1999
Src family kinases are required for integrin but not PDGFR signal transduction.
Article in The EMBO journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 283 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
283 citing papers in PubMed, 729 citations in OpenAlex.
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- Fibrinogen triggers perivascular fibroblast activation in a mouse model of cortical ischemic stroke.iScience · 2025Article
- Article
- Matrix-associated extracellular vesicles modulate smooth muscle cell adhesion and directionality by presenting collagen VI.bioRxiv : the preprint server for biology · 2025Article
- Mindin regulates fibroblast subpopulations through distinct Src family kinases during fibrogenesis.JCI insight · 2024Article
- DiverseGenes & development · 2024Article
- DiversebioRxiv : the preprint server for biology · 2024Article
- A renaissance for YES in cancer.Oncogene · 2023Review
- Phosphorylation of tyrosine 90 in SH3 domain is a new regulatory switch controlling Src kinase.eLife · 2023Article
- A back-door insight into the modulation of Src kinase activity by the polyamine spermidine.eLife · 2023Article
- PhosY-secretome profiling combined with kinase-substrate interaction screening defines active c-Src-driven extracellular signaling.Cell reports · 2023Article
- pYtags enable spatiotemporal measurements of receptor tyrosine kinase signaling in living cells.eLife · 2023Article
- Mitochondrial matrix-localized Src kinase regulates mitochondrial morphology.Cellular and molecular life sciences : CMLS · 2022Article
- Protein Kinase A in cellular migration-Niche signaling of a ubiquitous kinase.Frontiers in molecular biosciences · 2022Review
- Cell adhesion suppresses autophagy via Src/FAK-mediated phosphorylation and inhibition of AMPK.Cellular signalling · 2022Article
- Positive feedback between the T cell kinase Zap70 and its substrate LAT acts as a clustering-dependent signaling switch.Cell reports · 2021Article
- Regulation of Fibroblast Cell Polarity by Src Tyrosine Kinase.Biomedicines · 2021Article
- Secretome Profiling of Atlantic Salmon Head Kidney Leukocytes Highlights the Role of Phagocytes in the Immune Response to Soluble β-Glucan.Frontiers in immunology · 2021Article
- Epidermal Growth Factor Receptor and Abl2 Kinase Regulate Distinct Steps of Human Papillomavirus 16 Endocytosis.Journal of virology · 2020Article
- MicroRNA-200 family governs ovarian inclusion cyst formation and mode of ovarian cancer spread.Oncogene · 2020Article
223 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Src family kinases (SFKs) have been implicated as important regulators of ligand-induced cellular responses including proliferation, survival, adhesion and migration. Analysis of SFK function has been impeded by extensive redundancy between family members. We have generated mouse embryos harboring functional null mutations of the ubiquitously expressed SFKs Src, Yes and Fyn. This triple mutation leads to severe developmental defects and lethality by E9.5. To elucidate the molecular mechanisms underlying this phenotype, SYF cells (deficient for Src, Yes and Fyn) were derived and tested for their ability to respond to growth factors or plating on extracellular matrix. Our studies reveal that while Src, Yes and Fyn are largely dispensable for platelet-derived growth factor (PDGF)-induced signaling, they are absolutely required to mediate specific functions regulated by extracellular matrix proteins. Fibronectin-induced tyrosine phosphorylation of focal adhesion proteins, including the focal adhesion kinase FAK, was nearly eliminated in the absence of Src, Yes and Fyn. Furthermore, consistent with previous reports demonstrating the importance of FAK for cell migration, SYF cells displayed reduced motility in vitro. These results demonstrate that SFK activity is essential during embryogenesis and suggest that defects observed in SYF triple mutant embryos may be linked to deficiencies in signaling by extracellular matrix-coupled receptors.
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What Socratic 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 Socratic graph.