ArticleDevelopment (Cambridge, England)2009
Convergent extension movements in growth plate chondrocytes require gpi-anchored cell surface proteins.
Article in Development (Cambridge, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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
29 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- N-cadherin and β1 integrin coordinately regulate growth plate cartilage architecture.Molecular biology of the cell · 2024Article
- Cellular basis of differential endochondral growth in Lake Malawi cichlids.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Article
- Multiple morphogens and rapid elongation promote segmental patterning during development.PLoS computational biology · 2021Article
- A CRISPR-Cas9-engineered mouse model for GPI-anchor deficiency mirrors human phenotypes and exhibits hippocampal synaptic dysfunctions.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- CNS glycosylphosphatidylinositol deficiency results in delayed white matter development, ataxia and premature death in a novel mouse model.Human molecular genetics · 2020Article
- Continuous Dynamic Modeling of Regulated Cell Adhesion: Sorting, Intercalation, and Involution.Biophysical journal · 2019Article
- Proteome analysis of human mesenchymal stem cells undergoing chondrogenesis when exposed to the products of various magnesium-based materials degradation.Bioactive materials · 2019Article
- Article
- Discs large 1 controls daughter-cell polarity after cytokinesis in vertebrate morphogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- A Tunable, Three-Dimensional In Vitro Culture Model of Growth Plate Cartilage Using Alginate Hydrogel Scaffolds.Tissue engineering. Part A · 2018Article
- Article
- Glypican-6 promotes the growth of developing long bones by stimulating Hedgehog signaling.The Journal of cell biology · 2017Article
- A novel role of the organizer gene Goosecoid as an inhibitor of Wnt/PCP-mediated convergent extension in Xenopus and mouse.Scientific reports · 2017Article
- INPPL1 gene mutations in opsismodysplasia.Journal of human genetics · 2017Review
- A Novel Role for the BMP Antagonist Noggin in Sensitizing Cells to Non-canonical Wnt-5a/Ror2/Disheveled Pathway Activation.Frontiers in cell and developmental biology · 2017Article
- Dynamic imaging of the growth plate cartilage reveals multiple contributors to skeletal morphogenesis.Nature communications · 2015Article
- Article
- A dynamic cell adhesion surface regulates tissue architecture in growth plate cartilage.Development (Cambridge, England) · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Proteins that are localized to the cell surface via glycosylphosphatidylinositol (gpi) anchors have been proposed to regulate cell signaling and cell adhesion events involved in tissue patterning. Conditional deletion of Piga, which encodes the catalytic subunit of an essential enzyme in the gpi-biosynthetic pathway, in the lateral plate mesoderm results in normally patterned limbs that display chondrodysplasia. Analysis of mutant and mosaic Piga cartilage revealed two independent cell autonomous defects. First, loss of Piga function interferes with signal reception by chondrocytes as evidenced by delayed maturation. Second, the proliferative chondrocytes, although present, fail to flatten and arrange into columns. We present evidence that the abnormal organization of mutant proliferative chondrocytes results from errors in cell intercalation. Collectively, our data suggest that the distinct morphological features of the proliferative chondrocytes result from a convergent extension-like process that is regulated independently of chondrocyte maturation.
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.