ArticleCellular signalling2015
Cooperation of distinct Rac-dependent pathways to stabilise E-cadherin adhesion.
Article in Cellular signalling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 21 citations in OpenAlex.
- E-Cadherin: A conductor of cellular signaling.Current opinion in cell biology · 2025Review
- Prickle2 regulates apical junction remodeling and tissue fluidity during vertebrate neurulation.The Journal of cell biology · 2025Article
- Liraglutide Promotes Diabetic Wound Healing via Myo1c/Dock5.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Downregulation of Epidermal Growth Factor Receptor in hepatocellular carcinoma facilitates Transforming Growth Factor-β-induced epithelial to amoeboid transition.Cancer letters · 2019Article
- Epidermal activation of the small GTPase Rac1 in psoriasis pathogenesis.Small GTPases · 2019Review
- Adherens Junctions and Desmosomes Coordinate Mechanics and Signaling to Orchestrate Tissue Morphogenesis and Function: An Evolutionary Perspective.Cold Spring Harbor perspectives in biology · 2018Review
- Signaling by Small GTPases at Cell-Cell Junctions: Protein Interactions Building Control and Networks.Cold Spring Harbor perspectives in biology · 2018Review
- Cell-Cell Contact and Receptor Tyrosine Kinase Signaling.Cold Spring Harbor perspectives in biology · 2018Review
- KIF22 coordinates CAR and EGFR dynamics to promote cancer cell proliferation.Science signaling · 2018Article
- E-cadherin integrates mechanotransduction and EGFR signaling to control junctional tissue polarization and tight junction positioning.Nature communications · 2017Article
- Defining functional interactions during biogenesis of epithelial junctions.Nature communications · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The precise mechanisms via which Rac1 is activated by cadherin junctions are not fully known. In keratinocytes Rac1 activation by cadherin junctions requires EGFR signalling, but how EGFR does so is unclear. To address which activator could mediate E-cadherin signalling to Rac1, we investigated EGFR and two Rac1 GEFs, SOS1 and DOCK180. EGFR RNAi prevented junction-induced Rac1 activation and led to fragmented localization of E-cadherin at cadherin contacts. In contrast, depletion of another EGFR family member, ErbB3, did not interfere with either process. DOCK180 RNAi, but not SOS1, prevented E-cadherin-induced Rac1 activation. However, in a strong divergence from EGFR RNAi phenotype, DOCK180 depletion did not perturb actin recruitment or cadherin localisation at junctions. Rather, reduced DOCK180 levels impaired the resistance to mechanical stress of pre-formed cell aggregates. Thus, within the same cell type, EGFR and DOCK180 regulate Rac1 activation by newly-formed contacts, but control separate cellular events that cooperate to stabilise junctions.
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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.