ArticlePrenatal diagnosis2017
Global transcriptome dysregulation in second trimester fetuses with FMR1 expansions.
Article in Prenatal diagnosis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Amniotic fluid cell-free transcriptome: a glimpse into fetal development and placental cellular dynamics during normal pregnancy.BMC medical genomics · 2020Trial
- Maternal whole blood mRNA signatures identify women at risk of early preeclampsia: a longitudinal study.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2021Article
- Cortical gyrification and its relationships with molecular measures and cognition in children with the FMR1 premutation.Scientific reports · 2020Article
- Amniotic fluid transcriptomics reflects novel disease mechanisms in fetuses with myelomeningocele.American journal of obstetrics and gynecology · 2017Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
objectiveWe tested the hypothesis that FMR1 expansions would result in global gene dysregulation as early as the second trimester of human fetal development.
methodUsing cell-free fetal RNA obtained from amniotic fluid supernatant and expression microarrays, we compared RNA levels in samples from fetuses with premutation or full mutation allele expansions with control samples.
resultsWe found clear signals of differential gene expression relating to a variety of cellular functions, including ubiquitination, mitochondrial function, and neuronal/synaptic architecture. Additionally, among the genes showing differential gene expression, we saw links to related diseases of intellectual disability and motor function. Finally, within the unique molecular phenotypes established for each mutation set, we saw clear signatures of mitochondrial dysfunction and disrupted neurological function. Patterns of differential gene expression were very different in male and female fetuses with premutation alleles.
conclusionThese results support a model for which genetic misregulation during fetal development may set the stage for late clinical manifestations of FMR1-related disorders. © 2016 John Wiley & Sons, Ltd.
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