ArticleScientific reports2017
AmotL2 integrates polarity and junctional cues to modulate cell shape.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 15 citations in OpenAlex.
- VE-cadherin interaction proteomics identifies ARVCF as stabilizer of endothelial adherens junctions.iScience · 2026Article
- Circ_0001461 Regulates Colorectal Cancer Growth, Movement and Immune Escape Through miR-532-3p/AMOTL2.Biochemical genetics · 2026Article
- Multi-omics analysis reveals gut microbiota-host transcriptomic remodeling associated with the protective effects of Lacticaseibacillus rhamnosus GG against rotavirus enteritis.Frontiers in cellular and infection microbiology · 2026Article
- Phosphorylation of tumour suppressor Amotl2 by IKBKE kinase promotes YAP1 signalling, enhancing glioblastoma growth.Frontiers in oncology · 2026Article
- Article
- MAGI1 inhibits the AMOTL2/p38 stress pathway and prevents luminal breast tumorigenesis.Scientific reports · 2021Article
- Article
- Hippo-YAP/TAZ signaling in angiogenesis.BMB reports · 2018Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The assembly of individual epithelial or endothelial cells into a tight cellular sheet requires stringent control of cell packing and organization. These processes are dependent on the establishment and further integration of cellular junctions, the cytoskeleton and the formation of apical-basal polarity. However, little is known how these subcellular events are coordinated. The (Angiomotin) Amot protein family consists of scaffold proteins that interact with junctional cadherins, polarity proteins and the cytoskeleton. In this report, we have studied how these protein complexes integrate to control cellular shapes consistent with organ function. Using gene-inactivating studies in zebrafish and cell culture systems in vitro, we show that Par3 to be essential for localization of AmotL2 to cellular junctions to associate with VE/E-cadherin and subsequently the organization of radial actin filaments. Our data provide mechanistic insight in how critical processes such as aortic lumen expansion as well as epithelial packing into hexagonal shapes are controlled.
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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.