ArticlePloS one2012
Neural crest cell survival is dependent on Rho kinase and is required for development of the mid face in mouse embryos.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 36 citations in OpenAlex.
- The role of Rho GTPases in facial morphogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Review
- Exploration of Dentition Development and Replacement in Two Forms of Mexican Tetra (Astyanax mexicanus).Anatomia, histologia, embryologia · 2025Article
- C1-linker region of PARG1 RhoGAP promotes the catalytic recognition fold of RhoA substrate.PloS one · 2025Article
- Morphological, electrophysiological, and molecular alterations in foetal noncompacted cardiomyopathy induced by disruption of ROCK signalling.Frontiers in cell and developmental biology · 2024Article
- Count Me in, Count Me out: Regulation of the Tooth Number via Three Directional Developmental Patterns.International journal of molecular sciences · 2023Review
- The cell surface hyaluronidase TMEM2 plays an essential role in mouse neural crest cell development and survival.PLoS genetics · 2022Article
- Rho Kinases in Embryonic Development and Stem Cell Research.Archivum immunologiae et therapiae experimentalis · 2022Review
- Symmetry and fluctuation of cell movements in neural crest-derived facial mesenchyme.Development (Cambridge, England) · 2021Article
- Non-syndromic Cleft Palate: An Overview on Human Genetic and Environmental Risk Factors.Frontiers in cell and developmental biology · 2020Review
- Disruption of embryonic ROCK signaling reproduces the sarcomeric phenotype of hypertrophic cardiomyopathy.JCI insight · 2019Article
- MAPK and PI3K signaling: At the crossroads of neural crest development.Developmental biology · 2018Review
- An integrated genomic approach for the study of mandibular prognathism in the European seabass (Dicentrarchus labrax).Scientific reports · 2016Article
- Unidirectional Eph/ephrin signaling creates a cortical actomyosin differential to drive cell segregation.The Journal of cell biology · 2016Article
- Molecular mechanisms of midfacial developmental defects.Developmental dynamics : an official publication of the American Association of Anatomists · 2016Review
- Combination of fasudil and celecoxib promotes the recovery of injured spinal cord in rats better than celecoxib or fasudil alone.Neural regeneration research · 2015Article
- Neural crest specification by inhibition of the ROCK/Myosin II pathway.Stem cells (Dayton, Ohio) · 2015Article
- Article
- Rho-associated coiled-coil containing kinases (ROCK): structure, regulation, and functions.Small GTPases · 2014Review
- Potential benefits of rho-kinase inhibition in arterial hypertension.Current hypertension reports · 2013Review
- Neural crest cells are required for correct positioning of the developing outflow cushions and pattern the arterial valve leaflets.Cardiovascular research · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Neural crest cells (NCC) give rise to much of the tissue that forms the vertebrate head and face, including cartilage and bone, cranial ganglia and teeth. In this study we show that conditional expression of a dominant-negative (DN) form of Rho kinase (Rock) in mouse NCC results in severe hypoplasia of the frontonasal processes and first pharyngeal arch, ultimately resulting in reduction of the maxilla and nasal bones and severe craniofacial clefting affecting the nose, palate and lip. These defects resemble frontonasal dysplasia in humans. Disruption of the actin cytoskeleton, which leads to abnormalities in cell-matrix attachment, is seen in the RockDN;Wnt1-cre mutant embryos. This leads to elevated cell death, resulting in NCC deficiency and hypoplastic NCC-derived craniofacial structures. Rock is thus essential for survival of NCC that form the craniofacial region. We propose that reduced NCC numbers in the frontonasal processes and first pharyngeal arch, resulting from exacerbated cell death, may be the common mechanism underlying frontonasal dysplasia.
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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.