ArticlePloS one2017
The ectodomain of cadherin-11 binds to erbB2 and stimulates Akt phosphorylation to promote cranial neural crest cell migration.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- HER2 deficiency causes a developmental disorder with growth retardation and craniofacial malformations.The Journal of clinical investigation · 2026Article
- Adam13 interacts with large protein complexes to regulate histone modification and gene expression.Frontiers in cell and developmental biology · 2026Article
- Up-Regulation of microRNA-424 Causes an Imbalance in AKT Phosphorylation and Impairs Enteric Neural Crest Cell Migration in Hirschsprung Disease.International journal of molecular sciences · 2023Article
- Time to go: neural crest cell epithelial-to-mesenchymal transition.Development (Cambridge, England) · 2022Review
- Mubritinib enhanced the inhibiting function of cisplatin in lung cancer by interfering with mitochondrial function.Thoracic cancer · 2022Article
- Lactic acid promotes metastatic niche formation in bone metastasis of colorectal cancer.Cell communication and signaling : CCS · 2021Article
- The road best traveled: Neural crest migration upon the extracellular matrix.Seminars in cell & developmental biology · 2020Review
- Cadherin-11 Is Required for Neural Crest Specification and Survival.Frontiers in physiology · 2020Article
- Exon level machine learning analyses elucidate novel candidate miRNA targets in an avian model of fetal alcohol spectrum disorder.PLoS computational biology · 2019Article
- Cellular organization and boundary formation in craniofacial development.Genesis (New York, N.Y. : 2000) · 2019Review
- Cadherin-6B proteolytic N-terminal fragments promote chick cranial neural crest cell delamination by regulating extracellular matrix degradation.Developmental biology · 2018Article
- N-cadherin provides aProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Cut loose and run: The complex role of ADAM proteases during neural crest cell development.Genesis (New York, N.Y. : 2000) · 2018Review
- From Neural Crest Development to Cancer and Vice Versa: How p75Frontiers in molecular neuroscience · 2018Review
- Cadherins function during the collective cell migration of Xenopus Cranial Neural Crest cells: revisiting the role of E-cadherin.Mechanisms of development · 2017Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
During development, a multi-potent group of cells known as the cranial neural crest (CNC) migrate to form craniofacial structures. Proper migration of these cells requires proteolysis of cell adhesion molecules, such as cadherins. In Xenopus laevis, preventing extracellular cleavage of cadherin-11 impairs CNC migration. However, overexpression of the soluble cleavage product (EC1-3) is capable of rescuing this phenotype. The mechanism by which EC1-3 promotes CNC migration has not been investigated until now. Here we show that EC1-3 stimulates phosphorylation of Akt, a target of PI3K, in X.laevis CNC. Through immunoprecipitation experiments, we determined that EC1-3 interacts with all ErbB receptors, PDGFRα, and FGFR1. Of these receptors, only ErbB2 was able to produce an increase in Akt phosphorylation upon treatment with a recombinant EC1-3. This increase was abrogated by mubritinib, an inhibitor of ErbB2. We were able to recapitulate this decrease in Akt phosphorylation in vivo by knocking down ErbB2 in CNC cells. Knockdown of the receptor also significantly reduced CNC migration in vivo. We confirmed the importance of ErbB2 and ErbB receptor signaling in CNC migration using mubritinib and canertinib, respectively. Mubritinib and the PI3K inhibitor LY294002 significantly decreased cell migration while canertinib nearly prevented it altogether. These data show that ErbB2 and Akt are important for CNC migration and implicate other ErbB receptors and Akt-independent signaling pathways. Our findings provide the first example of a functional interaction between the extracellular domain of a type II classical cadherin and growth factor receptors.
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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.