ArticleDevelopment (Cambridge, England)2020
Disruption of the nectin-afadin complex recapitulates features of the human cleft lip/palate syndrome CLPED1.
Article in Development (Cambridge, England), 2020. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Hemidesmosomes and Notch signaling regulate epidermal differentiation via delamination.Development (Cambridge, England) · 2026Article
- Ectodermal loss of ARHGAP29 alters epithelial morphology and disrupts murine palatogenesis.Development (Cambridge, England) · 2026Article
- Actomyosin contractility and a threshold of cadherin cell adhesion are required during tissue fusion.The Journal of cell biology · 2026Article
- Hemidesmosomes regulate epidermal differentiation during embryogenesis.bioRxiv : the preprint server for biology · 2025Article
- Damaging Mutations inThe Cleft palate-craniofacial journal : official publication of the American Cleft Palate-Craniofacial Association · 2024Article
- E-cadherin variants associated with oral facial clefts trigger aberrant cell motility in a REG1A-dependent manner.Cell communication and signaling : CCS · 2024Article
- Rare variants found in multiplex families with orofacial clefts: Does expanding the phenotype make a difference?American journal of medical genetics. Part A · 2023Article
- AGS3 antagonizes LGN to balance oriented cell divisions and cell fate choices in mammalian epidermis.eLife · 2023Article
- Critical roles of adherens junctions in diseases of the oral mucosa.Tissue barriers · 2023Article
- Revisiting the embryogenesis of lip and palate development.Oral diseases · 2022Review
- A unique form of collective epithelial migration is crucial for tissue fusion in the secondary palate and can overcome loss of epithelial apoptosis.Development (Cambridge, England) · 2022Article
- To Stick or Not to Stick: Adhesions in Orofacial Clefts.Biology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cleft palate (CP), one of the most common congenital conditions, arises from failures in secondary palatogenesis during embryonic development. Several human genetic syndromes featuring CP and ectodermal dysplasia have been linked to mutations in genes regulating cell-cell adhesion, yet mouse models have largely failed to recapitulate these findings. Here, we use
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.