ArticleHuman genetics2006
Familial molar tissues due to mutations in the inflammatory gene, NALP7, have normal postzygotic DNA methylation.
Article in Human genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01008501 (Genetic Studies in Gestational Trophoblastic Disease), which is not on this map. Cited by 9 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.
Genetic Studies in Gestational Trophoblastic Disease
Who cites it
9 citing papers in PubMed, 32 citations in OpenAlex.
- NLRP7: From inflammasome regulation to human disease.Immunology · 2021Review
- Alteration of Genomic Imprinting after Assisted Reproductive Technologies and Long-Term Health.Life (Basel, Switzerland) · 2021Review
- New developments in Silver-Russell syndrome and implications for clinical practice.Epigenomics · 2016Review
- NLRP7 affects trophoblast lineage differentiation, binds to overexpressed YY1 and alters CpG methylation.Human molecular genetics · 2014Article
- Deep bisulfite sequencing of aberrantly methylated loci in a patient with multiple methylation defects.PloS one · 2013Article
- Three-dimensional structure of the NLRP7 pyrin domain: insight into pyrin-pyrin-mediated effector domain signaling in innate immunity.The Journal of biological chemistry · 2010Article
- Germline mutation in NLRP2 (NALP2) in a familial imprinting disorder (Beckwith-Wiedemann Syndrome).PLoS genetics · 2009Article
- Nod-like receptors: cytosolic watchdogs for immunity against pathogens.PLoS pathogens · 2007Review
- Gender specific differences in levels of DNA methylation at selected loci from human total blood: a tendency toward higher methylation levels in males.Human genetics · 2007Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An imprinting disorder has been believed to underlie the etiology of familial biparental hydatidiform moles (HMs) based on the abnormal methylation or expression of imprinted genes in molar tissues. However, the extent of the epigenetic defect in these tissues and the developmental stage at which the disorder begins have been poorly defined. In this study, we assessed the extent of abnormal DNA methylation in two HMs caused by mutations in the recently identified 19q13.4 gene, NALP7. We demonstrate normal postzygotic DNA methylation patterns at major repetitive and long interspersed nuclear elements (LINEs), genes on the inactive X-chromosome, three-cancer related genes, and CpG rich regions surrounding the PEG3 differentially methylated region (DMR). Our data provide a comprehensive assessment of DNA methylation in familial molar tissues and indicate that abnormal DNA methylation in these tissues is restricted to imprinted DMRs. The known role of NALP7 in apoptosis and inflammation pinpoints previously unrecognized pathways that could directly or indirectly underlie the abnormal methylation of imprinted genes in molar tissues.
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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.