ArticleThe Journal of cell biology2004
Cortactin and Crk cooperate to trigger actin polymerization during Shigella invasion of epithelial cells.
Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 84 citations in OpenAlex.
- Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024Review
- RACK1 promotesiScience · 2023Article
- Crosstalk between integrin/FAK and Crk/Vps25 governs invasion of bovine mammary epithelial cells byiScience · 2023Article
- Airway Epithelial Cell Junctions as Targets for Pathogens and Antimicrobial Therapy.Pharmaceutics · 2022Review
- Respiratory syncytial virus disrupts the airway epithelial barrier by decreasing cortactin and destabilizing F-actin.Journal of cell science · 2022Article
- Cortactin Promotes Effective AGS Cell Scattering byPathogens (Basel, Switzerland) · 2021Article
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- Airway tight junctions as targets of viral infections.Tissue barriers · 2021Article
- Epidermal Growth Factor Receptor and Abl2 Kinase Regulate Distinct Steps of Human Papillomavirus 16 Endocytosis.Journal of virology · 2020Article
- Bacteria That Cause Enteric Diseases Stimulate Distinct Humoral Immune Responses.Frontiers in immunology · 2020Review
- The Diverse Family of Arp2/3 Complexes.Trends in cell biology · 2017Review
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- Manipulation of host membranes by the bacterial pathogens Listeria, Francisella, Shigella and Yersinia.Seminars in cell & developmental biology · 2016Review
- Immunogenicity and Protective Response Induced by Recombinant Plasmids Based on the BAB1_0267 and BAB1_0270 Open Reading Frames ofFrontiers in cellular and infection microbiology · 2016Article
- Association between genetic polymorphisms in cortactin and susceptibility to gastric cancer.Annals of surgical treatment and research · 2015Article
- Identification of host proteins involved in rickettsial invasion of tick cells.Infection and immunity · 2015Article
- The Role of Crk Adaptor Proteins in T-Cell Adhesion and Migration.Frontiers in immunology · 2015Review
- p130Cas scaffolds the signalosome to direct adaptor-effector cross talk during Kaposi's sarcoma-associated herpesvirus trafficking in human microvascular dermal endothelial cells.Journal of virology · 2014Article
- Glycogen synthase kinase-3β stabilizes the interleukin (IL)-22 receptor from proteasomal degradation in murine lung epithelia.The Journal of biological chemistry · 2014Article
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 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shigella, the causative agent of bacillary dysentery, invades epithelial cells in a process involving Src tyrosine kinase signaling. Cortactin, a ubiquitous actin-binding protein present in structures of dynamic actin assembly, is the major protein tyrosine phosphorylated during Shigella invasion. Here, we report that RNA interference silencing of cortactin expression, as does Src inhibition in cells expressing kinase-inactive Src, interferes with actin polymerization required for the formation of cellular extensions engulfing the bacteria. Shigella invasion induced the recruitment of cortactin at plasma membranes in a tyrosine phosphorylation-dependent manner. Overexpression of wild-type forms of cortactin or the adaptor protein Crk favored Shigella uptake, and Arp2/3 binding-deficient cortactin derivatives or an Src homology 2 domain Crk mutant interfered with bacterial-induced actin foci formation. Crk was shown to directly interact with tyrosine-phosphorylated cortactin and to condition cortactin-dependent actin polymerization required for Shigella uptake. These results point at a major role for a Crk-cortactin complex in actin polymerization downstream of tyrosine kinase signaling.
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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.