about
The Prader-Willi syndrome protein necdin interacts with the E1A-like inhibitor of differentiation EID-1 and promotes myoblast differentiationTissue-specific and imprinted epigenetic modifications of the human NDN geneThe necdin gene is deleted in Prader-Willi syndrome and is imprinted in human and mouseA mouse model for Prader-Willi syndrome imprinting-centre mutationsMagel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cellsEssential role for the Prader-Willi syndrome protein necdin in axonal outgrowthDisruption of the mouse necdin gene results in early post-natal lethalityLoss of magel2, a candidate gene for features of Prader-Willi syndrome, impairs reproductive function in mice.Stochastic loss of silencing of the imprinted Ndn/NDN allele, in a mouse model and humans with prader-willi syndrome, has functional consequences.Long-range organization of tandem arrays of alpha satellite DNA at the centromeres of human chromosomes: high-frequency array-length polymorphism and meiotic stability.The Smc5/Smc6/MAGE complex confers resistance to caffeine and genotoxic stress in Drosophila melanogaster.Impaired hypothalamic regulation of endocrine function and delayed counterregulatory response to hypoglycemia in Magel2-null mice.Physical map of the centromeric region of human chromosome 7: relationship between two distinct alpha satellite arrays.Necdin, a p53 target gene, regulates the quiescence and response to genotoxic stress of hematopoietic stem/progenitor cells.Claudin-4 forms a paracellular barrier, revealing the interdependence of claudin expression in the loose epithelial cell culture model opossum kidney cells.Partial deletion of alpha satellite DNA associated with reduced amounts of the centromere protein CENP-B in a mitotically stable human chromosome rearrangement.Necdin, a Prader-Willi syndrome candidate gene, regulates gonadotropin-releasing hormone neurons during development.Targeting the endocannabinoid/CB1 receptor system for treating obesity in Prader-Willi syndrome.Leptin signaling defects in a mouse model of Prader-Willi syndrome: An orphan genetic obesity syndrome no more?Co-morbidity of complex genetic disorders and hypersomnias of central origin: lessons from the underlying neurobiology of wake and sleep.Loss of the Prader-Willi obesity syndrome protein necdin promotes adipogenesis.Establishment and maintenance of DNA methylation patterns in mouse Ndn: implications for maintenance of imprinting in target genes of the imprinting center.Magel2-null mice are hyper-responsive to setmelanotide, a melanocortin 4 receptor agonist.Expression of the Fanconi anemia gene FAC in human cell lines: lack of effect of oxygen tension.Evaluation of melanoma antigen (MAGE) gene expression in human cancers using The Cancer Genome Atlas.Human centromeric DNAs.An imprinted mouse transcript homologous to the human imprinted in Prader-Willi syndrome (IPW) gene.Regionally reduced brain volume, altered serotonin neurochemistry, and abnormal behavior in mice null for the circadian rhythm output gene Magel2.Structure of DNA near long tandem arrays of alpha satellite DNA at the centromere of human chromosome 7.Sleeve gastrectomy leads to weight loss in the Magel2 knockout mouse.Genetic analysis of very obese children with autism spectrum disorder.The Prader-Willi syndrome proteins MAGEL2 and necdin regulate leptin receptor cell surface abundance through ubiquitination pathways.Dopamine pathway imbalance in mice lacking Magel2, a Prader-Willi syndrome candidate gene.Loss of Necdin impairs myosin activation and delays cell polarization.Cloning and analysis of the murine Fanconi anemia group C cDNA.A MAGE/NDN-like gene in zebrafish.Prader-Willi syndrome transcripts are expressed in phenotypically significant regions of the developing mouse brain.Progressive postnatal decline in leptin sensitivity of arcuate hypothalamic neurons in the Magel2-null mouse model of Prader-Willi syndrome.Genome-wide analysis of gene transcription in the hypothalamus.Muscle dysfunction caused by loss of Magel2 in a mouse model of Prader-Willi and Schaaf-Yang syndromes.
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description
Canadees geneticus
@nl
Canadian geneticist
@en
Canadian geneticist
@en-ca
Canadian geneticist
@en-gb
genetista canadiense
@es
kanadische Professorin und Genetikerin
@de
عالمة وراثة كندية
@ar
name
Rachel Wevrick
@ast
Rachel Wevrick
@ca
Rachel Wevrick
@en
Rachel Wevrick
@es
Rachel Wevrick
@fr
Rachel Wevrick
@ga
Rachel Wevrick
@nl
Rachel Wevrick
@sl
Rachel Wevrick
@sq
type
label
Rachel Wevrick
@ast
Rachel Wevrick
@ca
Rachel Wevrick
@en
Rachel Wevrick
@es
Rachel Wevrick
@fr
Rachel Wevrick
@ga
Rachel Wevrick
@nl
Rachel Wevrick
@sl
Rachel Wevrick
@sq
prefLabel
Rachel Wevrick
@ast
Rachel Wevrick
@ca
Rachel Wevrick
@en
Rachel Wevrick
@es
Rachel Wevrick
@fr
Rachel Wevrick
@ga
Rachel Wevrick
@nl
Rachel Wevrick
@sl
Rachel Wevrick
@sq
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Rachel_Wevrick
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0000-0002-3343-5794
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