ReviewInternational journal of obesity (2005)2010
The role of GNAS and other imprinted genes in the development of obesity.
Review in International journal of obesity (2005), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
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Who cites it
48 citing papers in PubMed, 87 citations in OpenAlex.
- Acute sleep loss results in tissue-specific alterations in genome-wide DNA methylation state and metabolic fuel utilization in humans.Science advances · 2018Trial
- Analysis of Multiple Families With Single Individuals Affected by Pseudohypoparathyroidism Type Ib (PHP1B) Reveals Only One Novel Maternally Inherited GNAS Deletion.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016Trial
- Maternal Nutrient Restriction Programs Fetal Hepatic DNA Methylation in Ovine Monozygotic Twins.International journal of molecular sciences · 2026Article
- Temporal control of eating and body weight by GHSR-expressing suprachiasmatic nucleus neurons.Cell reports · 2025Article
- Genetic variants of accessory proteins and G proteins in human genetic disease.Critical reviews in clinical laboratory sciences · 2025Review
- Genome-wide screening reveals essential roles for HOX genes and imprinted genes during caudal neurogenesis of human embryonic stem cells.Stem cell reports · 2024Article
- Sex-specific transgenerational effects on murine thyroid gland imposed by ancestral exposure to neonicotinoid thiacloprid.Scientific reports · 2024Article
- Investigating the potential of single-cell DNA methylation data to detect allele-specific methylation and imprinting.American journal of human genetics · 2024Article
- Pseudohypoparathyroidism: complex disease variants with unfortunate names.Journal of molecular endocrinology · 2024Review
- Circulating Neuronatin Levels Are Positively Associated with BMI and Body Fat Mass but Not with Psychological Parameters.Nutrients · 2023Article
- Competition between stochastic neuropeptide signals calibrates the rate of satiation.Research square · 2023Article
- DNA methylation may affect beef tenderness through signal transduction in Bos indicus.Epigenetics & chromatin · 2022Article
- Variable allelic expression of imprinted genes at theFrontiers in cell and developmental biology · 2022Article
- Adipocyte-specific deletion of HuR induces spontaneous cardiac hypertrophy and fibrosis.American journal of physiology. Heart and circulatory physiology · 2021Article
- Molecular Definition of Pseudohypoparathyroidism Variants.The Journal of clinical endocrinology and metabolism · 2021Review
- A Novel GNAS Duplication Associated With Loss-of-Methylation Restricted to Exon A/B Causes Pseudohypoparathyroidism Type Ib (PHP1B).Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Perinatal DEHP exposure induces sex- and tissue-specific DNA methylation changes in both juvenile and adult mice.Environmental epigenetics · 2021Article
- Genome-wide profiling of DNA methylation and gene expression identifies candidate genes for human diabetic neuropathy.Clinical epigenetics · 2020Article
- Methplotlib: analysis of modified nucleotides from nanopore sequencing.Bioinformatics (Oxford, England) · 2020Article
- Searching for parent-of-origin effects on cardiometabolic traits in imprinted genomic regions.European journal of human genetics : EJHG · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Genomic imprinting is an epigenetic phenomenon affecting a small number of genes, which leads to differential expression from the two parental alleles. Imprinted genes are known to regulate fetal growth and a 'kinship' or 'parental conflict' model predicts that paternally and maternally expressed imprinted genes promote and inhibit fetal growth, respectively. In this review we examine the role of imprinted genes in postnatal growth and metabolism, with an emphasis on the GNAS/Gnas locus. GNAS is a complex imprinted locus with multiple oppositely imprinted gene products, including the G-protein alpha-subunit G(s)alpha that is expressed primarily from the maternal allele in some tissues and the G(s)alpha isoform XLalphas that is expressed only from the paternal allele. Maternal, but not paternal, G(s)alpha mutations lead to obesity in Albright hereditary osteodystrophy. Mouse studies show that this phenomenon is due to G(s)alpha imprinting in the central nervous system leading to a specific defect in the ability of central melanocortins to stimulate sympathetic nervous system activity and energy expenditure. In contrast mutation of paternally expressed XLalphas leads to opposite metabolic effects in mice. Although these findings conform to the 'kinship' model, the effects of other imprinted genes on body weight regulation do not conform to this model.
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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.