ArticleThe Journal of cell biology2018
Branched actin networks push against each other at adherens junctions to maintain cell-cell adhesion.
Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
What it found
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Who cites it
95 citing papers in PubMed, 141 citations in OpenAlex.
- FGD1 restrains actomyosin contractility to promote suprabasal junction maturation in stratified keratinocytes.Journal of cell science · 2026Article
- Nanoscale junctional membrane curvatures recruit BIN1 and SNX9 for endothelial collective migration.The Journal of cell biology · 2026Article
- Curving Actin Across Systems: Do Axonal Actin Rings Share Common Underlying Mechanisms?Journal of neurochemistry · 2026Review
- Spontaneous membrane protrusion and cell morphogenesis via self-propelled actin filaments.EMBO reports · 2026Article
- VE-Cadherin-Actin Regulation Promotes Mechanotransduction and Monolayer Maturation Involving a Tension-Sensitive Intermediate State.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Leader cell myosin 10 controls adhesion dynamics, invasion, and EMT pathway activation.Cell communication and signaling : CCS · 2026Article
- Actin-membrane interface stress regulates Arp2/3-branched actin density during lamellipodial protrusion.bioRxiv : the preprint server for biology · 2026Article
- Identification of PKN2 and MOB4 as Coordinators of Collective Cell Migration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Actomyosin-dependent assembly of the mechanosensitive machinery from adherens junctions triggers actin polymerization and organization.Science advances · 2026Article
- Alteration of Essential Cell Function by Ultrasound-Targeted Microbubble Cavitation.Current cardiology reports · 2025Review
- Actin filament assembly driven by distributive polymerases clustered on membrane surfaces.bioRxiv : the preprint server for biology · 2025Article
- Article
- A multicellular star-shaped actin network underpins epithelial organization and connectivity.Nature communications · 2025Article
- Cadherin dynamics and cortical tension in remodeling cell-cell adhesion during EMT.Biophysical journal · 2025Article
- The tumor suppressor RASSF8: A WAVE interaction partner controlling migration and cohesion of invasive border cells inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cell signaling facilitates apical constriction by basolaterally recruiting Arp2/3 via Rac and WAVE.The Journal of cell biology · 2025Article
- Membrane-associated polymerases deliver most of the actin subunits to a lamellipodial network.bioRxiv : the preprint server for biology · 2025Article
- A feedback circuitry involving γ-actin, β-actin and nonmuscle myosin-2 A controls tight junction and apical cortex mechanics.Nature communications · 2025Article
- Dysfunctional mechanotransduction regulates the progression of PIK3CA-driven vascular malformations.APL bioengineering · 2025Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Adherens junctions (AJs) are mechanosensitive cadherin-based intercellular adhesions that interact with the actin cytoskeleton and carry most of the mechanical load at cell-cell junctions. Both Arp2/3 complex-dependent actin polymerization generating pushing force and nonmuscle myosin II (NMII)-dependent contraction producing pulling force are necessary for AJ morphogenesis. Which actin system directly interacts with AJs is unknown. Using platinum replica electron microscopy of endothelial cells, we show that vascular endothelial (VE)-cadherin colocalizes with Arp2/3 complex-positive actin networks at different AJ types and is positioned at the interface between two oppositely oriented branched networks from adjacent cells. In contrast, actin-NMII bundles are located more distally from the VE-cadherin-rich zone. After Arp2/3 complex inhibition, linear AJs split, leaving gaps between cells with detergent-insoluble VE-cadherin transiently associated with the gap edges. After NMII inhibition, VE-cadherin is lost from gap edges. We propose that the actin cytoskeleton at AJs acts as a dynamic push-pull system, wherein pushing forces maintain extracellular VE-cadherin transinteraction and pulling forces stabilize intracellular adhesion complexes.
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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.