ArticleOncogene2014
Essential roles of Crk and CrkL in fibroblast structure and motility.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Development of Antagonist Peptides of the Crk/CrkL SH2 Domains by Modifying the Peripheral Amino Acid Residues of the YXXP Motif.Biochemistry · 2026Article
- R2HaPpY: Rapid-robust phosphotyrosine peptide enrichment using HaloTag-Src SH2 pY superbinder.bioRxiv : the preprint server for biology · 2025Article
- The p130Cas-Crk/CrkL Axis: A Therapeutic Target for Invasive Cancers Unveiled by Collaboration Among p130Cas, Crk, and CrkL.International journal of molecular sciences · 2025Review
- Use of phosphotyrosine-containing peptides to target SH2 domains: Antagonist peptides of the Crk/CrkL-p130Cas axis.Methods in enzymology · 2024Article
- Refining the Clinical Spectrum of the 17p13.3 Microduplication Syndrome: Case-Report of a Familial Small Microduplication.Biomedicines · 2022Article
- Crk and Crkl have shared functions in neural crest cells for cardiac outflow tract septation and vascular smooth muscle differentiation.Human molecular genetics · 2022Article
- Crk adaptor proteins are necessary for the development of the zebrafish retina.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Pyk2 regulates cell-edge protrusion dynamics by interacting with Crk.Molecular biology of the cell · 2021Article
- Depletion of Arg/Abl2 improves endothelial cell adhesion and prevents vascular leak during inflammation.Angiogenesis · 2021Article
- Review
- Fibroblast growth factor signalling in osteoarthritis and cartilage repair.Nature reviews. Rheumatology · 2020Review
- CrkL is required for donor T cell migration to GvHD target organs.Oncotarget · 2020Article
- The Crk adapter protein is essential forMolecular biology of the cell · 2019Article
- PEAK3/C19orf35 pseudokinase, a new NFK3 kinase family member, inhibits CrkII through dimerization.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Overexpression of CrkL as a novel biomarker for poor prognosis in gastric cancer.Cancer biomarkers : section A of Disease markers · 2019Article
- Crk adaptor proteins mediate actin-dependent T cell migration and mechanosensing induced by the integrin LFA-1.Science signaling · 2018Article
- An in silico proteomics screen to predict and prioritize protein-protein interactions dependent on post-translationally modified motifs.Bioinformatics (Oxford, England) · 2018Article
- IL-7-induced phosphorylation of the adaptor Crk-like and other targets.Cellular signalling · 2018Article
- Dynamic multi-site phosphorylation by Fyn and Abl drives the interaction between CRKL and the novel scaffolding receptors DCBLD1 and DCBLD2.The Biochemical journal · 2017Article
- Fibroblast Growth Requires CT10 Regulator of Kinase (Crk) and Crk-like (CrkL).The Journal of biological chemistry · 2016Article
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
Cytosolic proteins containing SH2 and SH3 domains, such as Crk and Crk-like (CrkL), are broadly expressed adapters that interact with a variety of proteins to fulfill key roles in signal transduction pathways triggered by activation of receptor and non-receptor tyrosine kinases. Crk and CrkL are similar to each other in structure and biochemical function, although they provide both distinct, as well as overlapping, biological roles during development. We developed a systematic approach to investigate Crk family functions at the cellular level by generating a conditional knock-out system for ablation of Crk and CrkL in cultured fibroblasts. The loss of both Crk and CrkL from fibroblasts resulted in reduced cell surface area and adoption of a rounded, refractile cellular phenotype. These morphological alterations were accompanied by a decrease in focal adhesion sites, reduced actin stress fibers and a collapse of microtubule structures. In addition, cells exhibited decreases in spontaneous motility and wound-healing behavior. Reduced p130Cas phosphorylation and actin levels closely followed the loss of Crk and CrkL, and stabilization of polymerized actin by jasplakinolide suppressed the morphological conversion. Ablation of Crk or CrkL alone conferred a much more modest phenotype suggesting that Crk and CrkL have overlapping functions that are critical for maintaining cell structure. The morphological alterations could be partially rescued by reintroduction of CrkII, and, to a lesser extent, CrkL. Taken together, our results suggest that Crk and CrkL have critical roles in cell structure and motility by maintaining cytoskeletal integrity.
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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.