ArticleThe EMBO journal1998
The catalytic activity of Src is dispensable for translocation to focal adhesions but controls the turnover of these structures during cell motility.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 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
106 citing papers in PubMed, 288 citations in OpenAlex.
- A noncommutative combinatorial protein logic circuit controls cell orientation in nanoenvironments.Science advances · 2023Article
- PPFIBP1 induces glioma cell migration and invasion through FAK/Src/JNK signaling pathway.Cell death & disease · 2021Article
- Regulation of Fibroblast Cell Polarity by Src Tyrosine Kinase.Biomedicines · 2021Article
- Up-regulated fibronectin in 3D culture facilitates spreading of triple negative breast cancer cells on 2D through integrin β-5 and Src.Scientific reports · 2019Article
- The role of APC-mediated actin assembly in microtubule capture and focal adhesion turnover.The Journal of cell biology · 2019Article
- Molecular Signature of Prospero Homeobox 1 (PROX1) in Follicular Thyroid Carcinoma Cells.International journal of molecular sciences · 2019Article
- The expression of Eps15 homology domain 1 is negatively correlated with disease-free survival and overall survival of osteosarcoma patients.Journal of orthopaedic surgery and research · 2019Article
- Long non-coding RNA PICSAR decreases adhesion and promotes migration of squamous carcinoma cells by downregulating α2β1 and α5β1 integrin expression.Biology open · 2018Article
- ΔNp63γ/SRC/Slug Signaling Axis Promotes Epithelial-to-Mesenchymal Transition in Squamous Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Redistribution of Adhesive Forces through Src/FAK Drives Contact Inhibition of Locomotion in Neural Crest.Developmental cell · 2018Article
- Adhesion structures in leukemia cells and their regulation by Src family kinases.Cell adhesion & migration · 2018Article
- Src-mediated tyrosine phosphorylation of Protein Kinase D2 at focal adhesions regulates cell adhesion.Scientific reports · 2017Article
- ARHGAP42 is activated by Src-mediated tyrosine phosphorylation to promote cell motility.Journal of cell science · 2017Article
- Autophagy in cancer metastasis.Oncogene · 2017Review
- p63 drives invasion in keratinocytes expressing HPV16 E6/E7 genes through regulation of Src-FAK signalling.Oncotarget · 2017Article
- Engineering extrinsic disorder to control protein activity in living cells.Science (New York, N.Y.) · 2016Article
- The ubiquitin-proteasome system regulates focal adhesions at the leading edge of migrating cells.eLife · 2016Article
- Autophagy Promotes Focal Adhesion Disassembly and Cell Motility of Metastatic Tumor Cells through the Direct Interaction of Paxillin with LC3.Cell reports · 2016Article
- PIAS1-FAK Interaction Promotes the Survival and Progression of Non-Small Cell Lung Cancer.Neoplasia (New York, N.Y.) · 2016Article
- A novel nuclear Src and p300 signaling axis controls migratory and invasive behavior in pancreatic cancer.Oncotarget · 2016Article
46 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
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Src family of protein tyrosine kinases is involved in transducing signals at sites of cellular adhesion. In particular, the v-Src oncoprotein resides in cellular focal adhesions, where it induces tyrosine phosphorylation of pp125FAK and focal adhesion loss during transformation. v-Src is translocated to cellular focal adhesions by an actin-dependent process. Here we have used mutant v-Src proteins that are temperature-dependent for translocation, but with secondary mutations that render them constitutively kinase-inactive or myristylation-defective, to show that neither v-Src kinase activity nor a myristyl group are required to induce association of v-Src with actin stress fibres and redistribution to sites of focal adhesions at the stress fibre termini. Moreover, switching the constitutively kinase-inactive or myristylation-defective temperature-sensitive v-Src proteins to the permissive temperature resulted in concomitant association with tyrosine-phosphorylated focal adhesion kinase (pp125FAK) and redistribution of both to focal adhesions. However, both catalytic activity and myristylation-mediated membrane association are required to induce dissociation of pp125FAK from v-Src, later degradation of pp125FAK and focal adhesion turnover during transformation and cell motility. These observations provide strong evidence that the role of the tyrosine kinase activity of the Src family at sites of cellular focal adhesions is to regulate the turnover of these structures during cell motility.
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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.