ArticleGenetics2004
Interactions between imprinting effects in the mouse.
Article in Genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 44 citations in OpenAlex.
- ZIM1 Combined with Hydrogel Inhibits Senescence of Primary PαS Cells during In Vitro Expansion.International journal of molecular sciences · 2023Article
- Snord116-dependent diurnal rhythm of DNA methylation in mouse cortex.Nature communications · 2018Article
- Regulatory links between imprinted genes: evolutionary predictions and consequences.Proceedings. Biological sciences · 2016Review
- A model for family-based case-control studies of genetic imprinting and epistasis.Briefings in bioinformatics · 2014Article
- The imprinted polycomb group gene Sfmbt2 is required for trophoblast maintenance and placenta development.Development (Cambridge, England) · 2013Article
- Cubilin expression is monoallelic and epigenetically augmented via PPARs.BMC genomics · 2013Article
- Evolution of genomic imprinting as a coordinator of coadapted gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Imprinting control region (ICR) of the Peg3 domain.Human molecular genetics · 2012Article
- Bayesian mapping of genome-wide epistatic imprinted loci for quantitative traits.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2012Article
- Genome-wide impact of a recently expanded microRNA cluster in mouse.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Postnatal survival of mice with maternal duplication of distal chromosome 7 induced by a Igf2/H19 imprinting control region lacking insulator function.PLoS genetics · 2010Article
- Unwitting hosts fall victim to imprinting.Epigenetics · 2008Article
- The PcG gene Sfmbt2 is paternally expressed in extraembryonic tissues.Gene expression patterns : GEP · 2008Article
- Article
- Cdkn1c (p57Kip2) is the major regulator of embryonic growth within its imprinted domain on mouse distal chromosome 7.BMC developmental biology · 2007Article
- Nondisjunction and transmission ratio distortion ofChromosome 2 in a (2.8) Robertsonian translocation mouse strain.Mammalian genome : official journal of the International Mammalian Genome Society · 2006Article
- Mapping of interactions and mouse congenic strains identified novel epistatic QTLs controlling the persistence of Salmonella Enteritidis in mice.Genes and immunity · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mice with uniparental partial or complete disomies for any one of 11 identified chromosomes show abnormal phenotypes. The abnormalities, or imprinting effects, can be attributable to an incorrect dosage of maternal or paternal copies of imprinted gene(s) located within the regions involved. Here we show that combinations of partial disomies may result in interactions between imprinting effects that seemingly independently affect fetal and/or placental growth in different ways or modify neonatal and postnatal imprinting effects. Candidate genes within the regions have been identified. The findings are generally in accord with the "conflict hypothesis" for the evolution of genomic imprinting but do not clearly demonstrate common growth axes within which imprinted genes may interact. Instead, it would seem that any gene that represses or limits embryonic/fetal growth to the advantage of the mother--by any developmental means--will have been subject to evolutionary selection for paternal allele repression. Likewise, any gene that favors embryonic/fetal development at consequent cost to the mother--by any developmental means--will have faced selection for maternal allele repression. The classical Igf2-Igf2r axis may therefore be unique. The findings involve reinterpretation of older imprinting data and consequently revision of the mouse imprinting map.
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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.