ReviewDisease models & mechanisms2020
Modeling human epigenetic disorders in mice: Beckwith-Wiedemann syndrome and Silver-Russell syndrome.
Review in Disease models & mechanisms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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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Who cites it
30 citing papers in PubMed, 61 citations in OpenAlex.
- Persistent postnatal IGF2 expression alters adult skeletal architecture inBone reports · 2026Article
- From renal development to pathology: An analysis of the multilevel role of insulin‑like growth factor 2 (Review).Molecular medicine reports · 2026Review
- Factors influencing the birth weight of ART-conceived offspring.Journal of assisted reproduction and genetics · 2025Review
- From Petri Dish to Primitive Heart: How IVF Alters Early Cardiac Gene Networks and Epigenetic Landscapes.Biomedicines · 2025Review
- Igf2 adult-specific skeletal muscle enhancer activity revealed in mice with intergenic CTCF boundary deletion.PLoS genetics · 2025Article
- Generation of human-induced pluripotent stem cells from a patient with Beckwith-Wiedemann syndrome.Human cell · 2025Article
- Insulin-Like Growth Factor 2 Reverses Synaptic and Cognitive Deficits in Fetal Growth Restriction Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Single-nucleus multiomic analysis of Beckwith-Wiedemann syndrome liver reveals PPARA signaling enrichment and metabolic dysfunction.Communications biology · 2025Article
- An obesogenic FTO allele causes accelerated development, growth and insulin resistance in human skeletal muscle cells.Nature communications · 2025Article
- Ventral body wall closure: Mechanistic insights from mouse models and translation to human pathology.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Review
- Skeletal stem/progenitor cell-derived rather than osteoblast-derived IGF2 supports the development and homeostasis of skeletal system via STAT3.International journal of biological sciences · 2025Article
- Polycomb function in early mouse development.Cell death and differentiation · 2025Review
- Joint effects of CD8A and ICOS in Long QT Syndrome (LQTS) and Beckwith-Wiedemann Syndrome (BWS).Journal of cardiothoracic surgery · 2024Article
- Imprinted DNA methylation of the H19 ICR is established and maintained in vivo in the absence of Kaiso.Epigenetics & chromatin · 2024Article
- Effects of Developmental Lead and Phthalate Exposures on DNA Methylation in Adult Mouse Blood, Brain, and Liver: A Focus on Genomic Imprinting by Tissue and Sex.Environmental health perspectives · 2024Article
- Article
- Prenatal diagnosis of a silver-russell syndrome caused by 11p15 duplication and pedigree analysis.Frontiers in genetics · 2024Article
- Epigenetic control of the imprinted growth regulatorEpigenetics · 2023Article
- DysregulatedeLife · 2022Article
- Epimutation in inherited metabolic disorders: the influence of aberrant transcription in adjacent genes.Human genetics · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Genomic imprinting, a phenomenon in which the two parental alleles are regulated differently, is observed in mammals, marsupials and a few other species, including seed-bearing plants. Dysregulation of genomic imprinting can cause developmental disorders such as Beckwith-Wiedemann syndrome (BWS) and Silver-Russell syndrome (SRS). In this Review, we discuss (1) how various (epi)genetic lesions lead to the dysregulation of clinically relevant imprinted loci, and (2) how such perturbations may contribute to the developmental defects in BWS and SRS. Given that the regulatory mechanisms of most imprinted clusters are well conserved between mice and humans, numerous mouse models of BWS and SRS have been generated. These mouse models are key to understanding how mutations at imprinted loci result in pathological phenotypes in humans, although there are some limitations. This Review focuses on how the biological findings obtained from innovative mouse models explain the clinical features of BWS and SRS.
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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.