ArticleMammalian genome : official journal of the International Mammalian Genome Society2004
Mapping a chromosomal locus for valproic acid-induced exencephaly in mice.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 21 citations in OpenAlex.
- Abnormal enteric nervous system organization and gastrointestinal motility in mice with valproic acid-induced neural tube defects.bioRxiv : the preprint server for biology · 2026Article
- Valproic Acid in Pregnancy Revisited: Neurobehavioral, Biochemical and Molecular Changes Affecting the Embryo and Fetus in Humans and in Animals: A Narrative Review.International journal of molecular sciences · 2023Review
- Gene-environment interactions underlying the etiology of neural tube defects.Current topics in developmental biology · 2023Article
- Embryonic Hypotaurine Levels Contribute to Strain-Dependent Susceptibility in Mouse Models of Valproate-Induced Neural Tube Defects.Frontiers in cell and developmental biology · 2022Article
- Unraveling the complex genetics of neural tube defects: From biological models to human genomics and back.Genesis (New York, N.Y. : 2000) · 2021Review
- Gene Environment Interactions in the Etiology of Neural Tube Defects.Frontiers in genetics · 2021Review
- Approaches to studying the genomic architecture of complex birth defects.Prenatal diagnosis · 2020Review
- Valproic acid disrupts the biomechanics of late spinal neural tube closure in mouse embryos.Mechanisms of development · 2018Article
- Cadmium-induced differential toxicogenomic response in resistant and sensitive mouse strains undergoing neurulation.Toxicological sciences : an official journal of the Society of Toxicology · 2009Article
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 5 institutions in 1 country.
Funding
Abstract
Human neural tube defects (NTDs) are among the most common congenital defects. They have a highly heterogeneous etiology, and, in addition to those seen in association with genetic syndromes, there are also NTDs induced by pharmaceutical compounds in utero, such as the widely used anti-epileptic drug valproic acid (VPA). Although familial studies have suggested a genetic contribution to VPA-induced NTDs, this trait has not been adequately studied, nor have the responsible genetic factors been identified. We generated a series of mouse crosses and backcrosses using the highly inbred SWV/Fnn and C57BL/6J strains, in order to identify possible chromosomal loci contributing to VPA sensitivity. When exposed to a high dose of sodium VPA (600 mg/kg) via maternal intraperitoneal injection on gestational day E8.5, the fetuses manifested exencephaly in a strain-dependent manner. Our data show an autosomal recessive trait, plus a gender-related effect or an overall X-Chromosome (Chr) effect, as being primarily responsible for determining sensitivity to VPA-induced exencephaly. Genome scanning and further linkage analysis of 131 exencephalic backcross fetuses identified a major locus linked to D7Mit285 (p < 2 x 10(-6)), exceeding the threshold for significant linkage. These results suggest a major chromosomal locus associated with the sensitivity to VPA-induced exencephaly in mice.
Indexed as
Identifiers
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.