ReviewMammalian genome : official journal of the International Mammalian Genome Society2011
The mouse notches up another success: understanding the causes of human vertebral malformation.
Review in Mammalian genome : official journal of the International Mammalian Genome Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Novel Splice Variant in theDiagnostics (Basel, Switzerland) · 2025Article
- Clinical genetics of spondylocostal dysostosis: A mini review.Frontiers in genetics · 2022Review
- Integration of Drosophila and Human Genetics to Understand Notch Signaling Related Diseases.Advances in experimental medicine and biology · 2018Review
- Small molecule screen in embryonic zebrafish using modular variations to target segmentation.Nature communications · 2017Article
- Osmotic and Heat Stress Effects on Segmentation.PloS one · 2016Article
- Novel ENU-Induced Mutation in Tbx6 Causes Dominant Spondylocostal Dysostosis-Like Vertebral Malformations in the Rat.PloS one · 2015Article
- Characterization of two ENU-induced mutations affecting mouse skeletal morphology.G3 (Bethesda, Md.) · 2013Article
- Notch and disease: a growing field.Seminars in cell & developmental biology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The defining characteristic of all vertebrates is a spine composed of a regular sequence of vertebrae. In humans, congenital spinal defects occur with an incidence of 0.5-1 per 1,000 live births and arise when the formation of vertebral precursors in the embryo is disrupted. These precursors (somites) form in a process (somitogenesis) in which each somite is progressively separated from an unsegmented precursor tissue. In the past decade the underlying genetic mechanisms driving this complex process have been dissected using animal models, revealing that it requires the coordinated action of at least 300 genes. Deletion of many of these genes in the mouse produces phenotypes with similar vertebral defects to those observed in human congenital abnormalities. This review highlights the role that such mouse models have played in the identification of the genetic causes of the malsegmentation syndrome spondylocostal dysostosis.
Indexed as
Identifiers
21667129What OpenQuestion 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 OpenQuestion graph.