Mechanisms regulating imprinted genes in clusters.
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Summary
Analysis of ICRs suggests that maternal and paternal methylation imprints function in distinct ways, and that Igf2/H19 locus is known to function as an insulator.
- Type
- review
- Published
- 2007-06-01
- Cited by
- 431
- References
- 86
- OpenAlex
- https://openalex.org/W1976695083
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:33335837
Keywords
Biology, Imprinting (psychology), Genomic imprinting, Promoter, DNA methylation
References
- A novel maternally expressed gene, ATP10C, encodes a putative aminophospholipid translocase associated with Angelman syndrome
- Bidirectional action of the Igf2r imprint control element on upstream and downstream imprinted genes.
- Methylation of a CTCF-dependent boundary controls imprinted expression of the Igf2 gene
- Dnmt3L and the Establishment of Maternal Genomic Imprints
- The essentials of DNA methylation.
- Active demethylation of the paternal genome in the mouse zygote.
- Differential regulation of imprinting in the murine embryo and placenta by the Dlk1-Dio3 imprinting control region
- Parental-origin-specific epigenetic modification of the mouse H19 gene
- Restricted co-expression of Dlk1 and the reciprocally imprinted non-coding RNA, Gtl2: implications for cis-acting control.
- Genomic imprinting contributes to thyroid hormone metabolism in the mouse embryo.
- Genomic imprinting: mother maintains methylation marks.
- PGC7/Stella protects against DNA demethylation in early embryogenesis
- A cluster of oppositely imprinted transcripts at the Gnas locus in the distal imprinting region of mouse chromosome 2.
- RNAi-mediated allelic trans-interaction at the imprinted Rtl1/Peg11 locus.
- The Angelman syndrome candidate gene, UBE3AIE6-AP, is imprinted in brain
- Tissue-specific expression of antisense and sense transcripts at the imprinted Gnas locus.
- Quantitative genetics: Turning up the heat on QTL mapping
- Limited evolutionary conservation of imprinting in the human placenta.
- A mouse model for Prader-Willi syndrome imprinting-centre mutations
- Imprinting along the Kcnq1 domain on mouse chromosome 7 involves repressive histone methylation and recruitment of Polycomb group complexes
Cited by
- Alterations in methylation and expression levels of imprinted genes H19 and Igf2 in the fetuses of diabetic mice.
- Coordinated diurnal regulation of genes from the Dlk1-Dio3 imprinted domain: implications for regulation of clusters of non-paralogous genes.
- Postnatal Changes in the Expression Pattern of the Imprinted Signalling Protein XLαs Underlie the Changing Phenotype of Deficient Mice
- Effects of maternal folic acid supplementation on gene methylation and being small for gestational age.
- PEG3 binds to H19-ICR as a transcriptional repressor
- Williams syndrome deletions and duplications: Genetic windows to understanding anxiety, sociality, autism, and schizophrenia
- Wnt/β-catenin signaling pathway safeguards epigenetic stability and homeostasis of mouse embryonic stem cells
- La réorganisation de la chromatine au cours de la spermatogénèse
- An ancestral regulatory mechanism underlies Hoxd gene expression in both developing genitals and digits
- Role of non-coding RNAs in pancreatic cancer: the bane of the microworld.
- In vitro culture of human embryos : effects on fetal development and the role of the placenta
- Chromatin architecture and the orchestration of gene expression: cell systems to explore epigenetic gene control
- Studying Niche Colonization and the Dynamics of Imprint Erasure During In Vitro Acquisition of Pluripotency in Germ Cells
- Évaluation du caryotype moléculaire en tant qu’outil diagnostique chez les enfants avec déficience intellectuelle et/ou malformations congénitales
- Role of CpG island methylation and MBD2 in immune cell gene regulation
- Characterization of macro non-protein-coding RNAs in the mouse genome
- Epigenetic regulation of stemness maintenance in the neurogenic niches.
- Phenotypic Consequences Of Imprinting Perturbations At Rasgrf1 In Mouse
- Développement de méthodes d'analyse de l'ADN par clivage d'une chimère ARN/ADN et par spectrométrie de masse MALDI-TOF
- Détermination de la structure secondaire d'une région de l'ARN Xist nécessaire à l'inactivation du chromosome X, la région des A-repeats, et identification de ses partenaires protéiques ayant un rôle structural ou fonctionnel dans l'inactivation
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