ArticleGenes & development1997
Mouse mutant embryos overexpressing IGF-II exhibit phenotypic features of the Beckwith-Wiedemann and Simpson-Golabi-Behmel syndromes.
Article in Genes & development, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
91 citing papers in PubMed, 341 citations in OpenAlex.
- Review
- From renal development to pathology: An analysis of the multilevel role of insulin‑like growth factor 2 (Review).Molecular medicine reports · 2026Review
- 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
- Trio-based GWAS identifies novel associations and subtype-specific risk factors for cleft palate.HGG advances · 2023Article
- Repurposing Normal Chromosomal Microarray Data to Harbor Genetic Insights into Congenital Heart Disease.Biology · 2023Article
- Imprinted Long Non-Coding RNAs in Mammalian Development and Disease.International journal of molecular sciences · 2023Review
- Trio-based GWAS identifies novel associations and subtype-specific risk factors for cleft palate.medRxiv : the preprint server for health sciences · 2023Article
- Possible transfer of lncRNA H19-derived miRNA miR-675-3p to adjacent H19-non-expressing trophoblast cells in near-term mouse placenta.Histochemistry and cell biology · 2023Article
- Long Noncoding RNAs: Recent Insights into Their Role in Male Infertility and Their Potential as Biomarkers and Therapeutic Targets.International journal of molecular sciences · 2021Review
- Variants in Maternal Effect Genes and Relaxed Imprinting Control in a Special Placental Mesenchymal Dysplasia Case with Mild Trophoblast Hyperplasia.Biomedicines · 2021Article
- Prenatal correction of IGF2 to rescue the growth phenotypes in mouse models of Beckwith-Wiedemann and Silver-Russell syndromes.Cell reports · 2021Article
- Discoidin Domain Receptor 1 functionally interacts with the IGF-I system in bladder cancer.Matrix biology plus · 2020Article
- Temporal regulation of prenatal embryonic development by paternal imprinted loci.Science China. Life sciences · 2020Article
- Article
- Maternal transmission of an Igf2r domain 11: IGF2 binding mutant allele (Igf2rScientific reports · 2019Article
- Placenta-specific epimutation at H19-DMR among common pregnancy complications: its frequency and effect on the expression patterns of H19 and IGF2.Clinical epigenetics · 2019Article
- The Emerging Role of Glucose Metabolism in Cartilage Development.Current osteoporosis reports · 2019Review
- Gene datasets associated with mouse cleft palate.Data in brief · 2018Article
- Genome-wide association study reveals a QTL and strong candidate genes for umbilical hernia in pigs on SSC14.BMC genomics · 2018Article
- IGF2 stimulates fetal growth in a sex- and organ-dependent manner.Pediatric research · 2018Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
In mice, the imprinted Igf2 gene (expressed from the paternal allele), which encodes a growth-promoting factor (IGF-II), is linked closely to the reciprocally imprinted H19 locus on chromosome 7. Also imprinted (expressed from the maternal allele) is the Igf2r gene on chromsome 17 encoding the type 2 IGF receptor that is involved in degradation of excess IGF-II. Double mutant embryos carrying a deletion around the H19 region and also a targeted Igf2r allele, both inherited maternally, have extremely high levels of IGF-II (7- and 11-fold higher than normal in tissues and serum, respectively) as a result of biallelic Igf2 expression (imprint relaxation by deletion of H19-associated sequence) in combination with lack of the IGF2R-mediated IGF-II turnover. This excess of IGF-II causes somatic overgrowth, visceromegaly, placentomegaly, omphalocele, and cardiac and adrenal defects, which are also features of the Beckwith-Wiedemann syndrome (BWS), a genetically complex human disorder associated with chromosomal abnormalities in the 11p15.5 region where the IGF2 gene resides. In addition, the double mutant mouse embryos exhibit skeletal defects and cleft palate, which are manifestations observed frequently in the Simpson-Golabi-Behmel syndrome, another overgrowth disorder overlapping phenotypically, but not genetically, with BWS.
Indexed as
Identifiers
What OpenQuestion holds
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.