ArticleAmerican journal of human genetics2005
Differential X reactivation in human placental cells: implications for reversal of X inactivation.
Article in American journal of human genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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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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.
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Who cites it
18 citing papers in PubMed.
- Mind the Litter: The Critical Role of Intralitter Variables in Reproductive and Developmental Toxicology Research.Birth defects research · 2026Review
- Sex-influenced DNA methylation differs by placental cell type.Biology of sex differences · 2026Article
- Placental biology links genetic, epigenetic, ancestral, and social determinants to maternal-fetal health inequities.Frontiers in reproductive health · 2026Review
- Paternal DDT exposure induces sex-specific programming of fetal growth, placenta development and offspring's health phenotypes in a mouse model.Scientific reports · 2024Article
- Sex-Specific Transcriptomic Changes in the Villous Tissue of Placentas of Pregnant Women Using a Selective Serotonin Reuptake Inhibitor.ACS chemical neuroscience · 2024Article
- The influence of fetal sex on antenatal maternal glucose and insulin dynamics.Frontiers in clinical diabetes and healthcare · 2024Review
- Disruption of O-Linked N-Acetylglucosamine Signaling in Placenta Induces Insulin Sensitivity in Female Offspring.International journal of molecular sciences · 2021Article
- The omniscient placenta: Metabolic and epigenetic regulation of fetal programming.Frontiers in neuroendocrinology · 2015Review
- The human placental methylome.Cold Spring Harbor perspectives in medicine · 2015Review
- Prenatal exposure to mixtures of xenoestrogens and repetitive element DNA methylation changes in human placenta.Environment international · 2014Article
- XCI in preimplantation mouse and human embryos: first there is remodelling….Human genetics · 2011Review
- Article
- Inactive X chromosome-specific reduction in placental DNA methylation.Human molecular genetics · 2009Article
- X chromosome inactivation is initiated in human preimplantation embryos.American journal of human genetics · 2009Article
- Candida glabrata PHO4 is necessary and sufficient for Pho2-independent transcription of phosphate starvation genes.Genetics · 2009Article
- Two novel connexin32 mutations cause early onset X-linked Charcot-Marie-Tooth disease.BMC neurology · 2007Article
- Hypermethylation of RASSF1A in human and rhesus placentas.The American journal of pathology · 2007Article
- X-chromosome inactivation patterns in females with Prader-Willi syndrome.American journal of medical genetics. Part A · 2007Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
X inactivation--the mammalian method of X chromosome dosage compensation--is extremely stable in human somatic cells; only fetal germ cells have a developmental program to reverse the process. The human placenta, at term, differs from other somatic tissues, since it has the ability to reverse the X-inactivation program. To determine whether reversal can be induced at other stages of placental development, we examined earlier placental specimens using a cell-hybridization assay. We found that global X reactivation is also inducible in villi cells from first-trimester spontaneous abortions but not from first-trimester elective terminations. These differences in inducibility are not associated with detectable variation in histone H4 acetylation, DNA methylation, or XIST expression--hallmarks of the inactivation process--so other factors must have a role. One notable feature is that the permissive cells, unlike nonpermissive ones, have ceased to proliferate in vivo and are either beginning or in the process of programmed cell death. Cessation of mitotic proliferation also characterizes oocytes at the stage at which they undergo X reactivation. We suggest that, along with undermethylation, the apoptotic changes accompanying cessation of cell proliferation contribute to the reversal of inactivation, not only in placental cells, but also in oocytes entering meiosis.
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Registered trials
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