ReviewBirth defects research. Part C, Embryo today : reviews2007
Retinoic acid regulation of the somitogenesis clock.
Review in Birth defects research. Part C, Embryo today : reviews, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 70 citations in OpenAlex.
- Pin1 Downregulation Is Involved in Excess Retinoic Acid-Induced Failure of Neural Tube Closure.International journal of molecular sciences · 2024Article
- The Clock and Wavefront Self-Organizing model recreates the dynamics of mouse somitogenesis in vivo and in vitro.Development (Cambridge, England) · 2024Article
- Patterning of vertebrate cardiac progenitor fields by retinoic acid signaling.Genesis (New York, N.Y. : 2000) · 2021Review
- Article
- Patterning with clocks and genetic cascades: Segmentation and regionalization of vertebrate versus insect body plans.PLoS genetics · 2021Review
- Comparative analysis of serum proteome in congenital scoliosis patients with TBX6 haploinsufficiency - a first report pointing to lipid metabolism.Journal of cellular and molecular medicine · 2018Article
- A novel de novo mutation in MYT1, the unique OAVS gene identified so far.European journal of human genetics : EJHG · 2017Article
- Congenital scoliosis in Smith-Magenis syndrome: a case report and review of the literature.Medicine · 2015Review
- Environmental aspects of congenital scoliosis.Environmental science and pollution research international · 2015Review
- Retinoic acid signaling pathways in development and diseases.Bioorganic & medicinal chemistry · 2014Review
- Retinoic acid actions through mammalian nuclear receptors.Chemical reviews · 2014Review
- Retinoic acid-dependent regulation of miR-19 expression elicits vertebrate axis defects.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Dhrs3 protein attenuates retinoic acid signaling and is required for early embryonic patterning.The Journal of biological chemistry · 2013Article
- Human cytochromes P450 in health and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013Review
- Article
- Article
- Growth differentiation factor 11 signaling controls retinoic acid activity for axial vertebral development.Developmental biology · 2010Article
- Interplay between activin and Hox genes determines the formation of the kidney morphogenetic field.Development (Cambridge, England) · 2009Article
- Developmental expression of retinoic acid receptors (RARs).Nuclear receptor signaling · 2009Review
- The expanding role for retinoid signaling in heart development.TheScientificWorldJournal · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Retinoic acid (RA) is a signaling molecule synthesized from vitamin A that controls gene expression at the transcriptional level by functioning as a ligand for nuclear RA receptors. RA plays an essential role during embryonic development in higher animals by regulating key genes involved in pattern formation. RA is required for induction of several Hox genes involved in patterning of the hindbrain and spinal cord as neuroectoderm emerges from the primitive streak. Recent findings indicate that RA is also required to ensure bilaterally symmetrical generation of left and right somites as presomitic mesoderm emerges from the primitive streak. RA may control somitogenesis through its ability to repress posterior ectodermal expression of fibroblast growth factor-8 (Fgf8) for a short period of time during the late primitive streak stage when the somitogenesis clock initiates. During this tight temporal window, RA is required to limit Fgf8 expression to the most posterior ectoderm (epiblast), thus preventing ectopic Fgf8 expression in more anterior ectoderm including the node ectoderm and neuroectoderm. Although Fgf8 is required for the node to impart left-right asymmetry on specific tissues (heart, visceral organs, etc.), excess Fgf8 signaling following a loss of RA may stimulate the node to generate asymmetry also in presomitic mesoderm, leading to left-right asymmetry in the somitogenesis clock. These findings suggest that human vertebral birth defects such as scoliosis, an abnormal left-right bending of the vertebral column, may be caused by a defect in RA signaling during somitogenesis.
Indexed as
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What 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.