ArticleDevelopmental biology2016
ADAM13 cleavage of cadherin-11 promotes CNC migration independently of the homophilic binding site.
Article in Developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Adam13 interacts with large protein complexes to regulate histone modification and gene expression.Frontiers in cell and developmental biology · 2026Article
- Comparative analysis of fixation techniques for signal detection in avian embryos.Developmental biology · 2025Article
- "Beyond transcription: How post-transcriptional mechanisms drive neural crest EMT".Genesis (New York, N.Y. : 2000) · 2024Review
- Cadherin-11 increases tumor cell proliferation and metastatic potential via Wnt pathway activation.Molecular oncology · 2023Article
- Tumour follower cells: A novel driver of leader cells in collective invasion (Review).International journal of oncology · 2023Review
- ADAM11 a novel regulator of Wnt and BMP4 signaling in neural crest and cancer.Frontiers in cell and developmental biology · 2023Article
- Time to go: neural crest cell epithelial-to-mesenchymal transition.Development (Cambridge, England) · 2022Review
- Lactic acid promotes metastatic niche formation in bone metastasis of colorectal cancer.Cell communication and signaling : CCS · 2021Article
- Plasma proteomic profiling of young and old mice reveals cadherin-13 prevents age-related bone loss.Aging · 2020Article
- 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
- Review
- Sperm capacitation is associated with phosphorylation of the testis-specific radial spoke protein Rsph6a†.Biology of reproduction · 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
- TBC1d24-ephrinB2 interaction regulates contact inhibition of locomotion in neural crest cell migration.Nature communications · 2018Article
- A catenin-dependent balance between N-cadherin and E-cadherin controls neuroectodermal cell fate choices.Mechanisms of development · 2018Article
- Cut loose and run: The complex role of ADAM proteases during neural crest cell development.Genesis (New York, N.Y. : 2000) · 2018Review
- Neural crest development in Xenopus requires Protocadherin 7 at the lateral neural crest border.Mechanisms of development · 2018Article
- Resolving in vivo gene expression during collective cell migration using an integrated RNAscope, immunohistochemistry and tissue clearing method.Mechanisms of development · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
Abstract
The cranial neural crest (CNC) is a highly motile population of cells that is responsible for forming the face and jaw in all vertebrates and perturbing their migration can lead to craniofacial birth defects. Cell motility requires a dynamic modification of cell-cell and cell-matrix adhesion. In the CNC, cleavage of the cell adhesion molecule cadherin-11 by ADAM13 is essential for cell migration. This cleavage generates a shed extracellular fragment of cadherin-11 (EC1-3) that possesses pro-migratory activity via an unknown mechanism. Cadherin-11 plays an important role in modulating contact inhibition of locomotion (CIL) in the CNC to regulate directional cell migration. Here, we show that while the integral cadherin-11 requires the homophilic binding site to promote CNC migration in vivo, the EC1-3 fragment does not. In addition, we show that increased ADAM13 activity or expression of the EC1-3 fragment increases CNC invasiveness in vitro and blocks the repulsive CIL response in colliding cells. This activity requires the presence of an intact homophilic binding site on the EC1-3 suggesting that the cleavage fragment may function as a competitive inhibitor of cadherin-11 adhesion in CIL but not to promote cell migration in vivo.
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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.