ArticleMolecular and cellular biology2000
Identification of a methylation imprint mark within the mouse Gnas locus.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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.
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Who cites it
72 citing papers in PubMed, 185 citations in OpenAlex.
- Imprinting and skeletal disorders: lessons from pseudohypoparathyroidism and related disorders.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Review
- A biallelically active embryonic enhancer dictates GNAS imprinting through allele-specific conformations.Nature communications · 2025Article
- Recurrent small variants in NESP55/NESPAS associated with broad GNAS methylation defects and pseudohypoparathyroidism type 1B.JCI insight · 2024Article
- DNA methylation of imprint control regions associated with Alzheimer's disease in non-Hispanic Blacks and non-Hispanic Whites.Clinical epigenetics · 2024Article
- Pseudohypoparathyroidism: complex disease variants with unfortunate names.Journal of molecular endocrinology · 2024Review
- The long-range interaction between two GNAS imprinting control regions delineates pseudohypoparathyroidism type 1B pathogenesis.The Journal of clinical investigation · 2023Article
- LncRNA GNAS-AS1 knockdown inhibits keloid cells growth by mediating the miR-188-5p/RUNX2 axis.Molecular and cellular biochemistry · 2023Article
- Article
- Targeted Long-Read Sequencing Identifies a Retrotransposon Insertion as a Cause of Altered GNAS Exon A/B Methylation in a Family With Autosomal Dominant Pseudohypoparathyroidism Type 1b (PHP1B).Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- DNA methylation dynamics and dysregulation delineated by high-throughput profiling in the mouse.Cell genomics · 2022Article
- Lack of GNAS Remethylation During Oogenesis May Be a Cause of Sporadic Pseudohypoparathyroidism Type Ib.The Journal of clinical endocrinology and metabolism · 2022Article
- High-throughput Molecular Analysis of Pseudohypoparathyroidism 1b Patients Reveals Novel Genetic and Epigenetic Defects.The Journal of clinical endocrinology and metabolism · 2021Article
- Somatotroph Tumors and the Epigenetic Status of theInternational journal of molecular sciences · 2021Article
- Molecular Definition of Pseudohypoparathyroidism Variants.The Journal of clinical endocrinology and metabolism · 2021Review
- ZFP57 dictates allelic expression switch of target imprinted genes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- MaternalFrontiers in genetics · 2021Article
- Article
- Neonatal McCune-Albright Syndrome: A Unique Syndromic Profile With an Unfavorable Outcome.JBMR plus · 2019Article
- The role of long non-coding RNAs in the pathogenesis of hereditary diseases.BMC medical genomics · 2019Review
- Heterotrimeric G proteins in the control of parathyroid hormone actions.Journal of molecular endocrinology · 2017Review
12 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
5 authors at 2 institutions in 1 country.
Funding
Abstract
The imprinted mouse gene Gnas produces the G protein alpha-subunit G(S)alpha and several other gene products by using alternative promoters and first exons. G(S)alpha is maternally expressed in some tissues and biallelically expressed in most other tissues, while the gene products NESP55 and XLalphas are maternally and paternally expressed, respectively. We investigated the mechanisms of Gnas imprinting. The G(S)alpha promoter and first exon are not methylated on either allele. A further upstream region (approximately from positions -3400 to -939 relative to the G(S)alpha translational start site) is methylated only on the maternal allele in all adult somatic tissues and in early postimplantation development. Within this region lies a fourth promoter and first exon (exon 1A) that generates paternal-specific mRNAs of unknown function. Exon 1A and G(S)alpha mRNAs have similar expression patterns, making competition between their promoters unlikely. Differential methylation in this region is established during gametogenesis, being present in oocytes and absent in spermatozoa, and is maintained in preimplantation E3. 5d blastocysts. Therefore, this region is a methylation imprint mark. In contrast, differential methylation of the NESP55 and XLalphas promoter regions (Nesp and Gnasxl) is not established during gametogenesis. The methylation imprint mark that we identified may be important for the tissue-specific imprinting of G(S)alpha.
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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.