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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

MAGE-like 2

Magel2, NDNL1, NS7
Prader-Willi syndrome (PWS) is caused by the loss of expression of imprinted genes in chromosome 15q11-q13 region. Affected individuals exhibit neonatal hypotonia, developmental delay, and childhood-onset obesity. Necdin (NDN), a gene involved in the terminal differentiation of neurons, localizes to this region of the genome and has been implicated as one of the genes responsible for the etiology of PWS. This gene is structurally similar to NDN, is also localized to the PWS chromosomal region, and is paternally imprinted, suggesting a possible role for it in PWS. [provided by RefSeq, Oct 2010] (from NCBI)
Top mentioned proteins: CAN, ACID, POLYMERASE, HAD, UBE3A
Papers on Magel2
Truncating Mutations of MAGEL2, a Gene within the Prader-Willi Locus, Are Responsible for Severe Arthrogryposis.
Melki et al., Le Kremlin-Bicêtre, France. In Am J Hum Genet, Nov 2015
By genetic mapping and whole-exome sequencing in a multiplex family, a heterozygous truncating MAGEL2 mutation leading to frameshift and a premature stop codon (c.1996delC, p.Gln666Serfs∗36) and inherited from the father was identified in the probands.
Progressive postnatal decline in leptin sensitivity of arcuate hypothalamic neurons in the Magel2-null mouse model of Prader-Willi syndrome.
Wevrick et al., Edmonton, Canada. In Hum Mol Genet, Sep 2015
De novo inactivating mutations in one PWS candidate gene, MAGEL2, have been identified in children with features of PWS. Adult mice lacking Magel2 are insensitive to the anorexic effect of leptin treatment, and their hypothalamic pro-opiomelanocortin (POMC) neurons fail to depolarize in response to leptin.
An Early Postnatal Oxytocin Treatment Prevents Social and Learning Deficits in Adult Mice Deficient for Magel2, a Gene Involved in Prader-Willi Syndrome and Autism.
Muscatelli et al., Toulouse, France. In Biol Psychiatry, Aug 2015
BACKGROUND: Mutations of MAGEL2 have been reported in patients presenting with autism, and loss of MAGEL2 is also associated with Prader-Willi syndrome, a neurodevelopmental genetic disorder.
The murine norovirus core subgenomic RNA promoter consists of a stable stem-loop that can direct accurate initiation of RNA synthesis.
Goodfellow et al., London, United Kingdom. In J Virol, Feb 2015
We have previously described the presence of an evolutionarily conserved RNA stem-loop structure on the negative-sense RNA, the complementary sequence of which codes for the viral RNA-dependent RNA polymerase (NS7).
Structure determination of Murine Norovirus NS6 proteases with C-terminal extensions designed to probe protease-substrate interactions.
Curry et al., London, United Kingdom. In Peerj, 2014
We report the crystallization and crystal structure determination of inactive mutants of murine norovirus NS6 protease with C-terminal extensions of one, two and four residues from the N-terminus of the adjacent NS7 protein (NS6 1', NS6 2', NS6 4').
Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.
Ong et al., Cambridge, United Kingdom. In Nature, 2014
Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns.
Promoter characterization and functional association with placenta of porcine MAGEL2.
Whitelaw et al., Chongqing, China. In Gene, 2014
MAGEL2 (melanoma antigen-like gene 2) is essential for circadian function, metabolism and reproduction in mammals.
Discovery of a novel bottlenose dolphin coronavirus reveals a distinct species of marine mammal coronavirus in Gammacoronavirus.
Yuen et al., Hong Kong, Hong Kong. In J Virol, 2014
Their genome size is about 32,000 nucleotides, the largest among all CoVs, as a result of multiple unique open reading frames (NS5a, NS5b, NS5c, NS6, NS7, NS8, NS9, and NS10) between their membrane (M) and nucleocapsid (N) protein genes.
Duplication of the 15q11-q13 region: clinical and genetic study of 30 new cases.
Verloes et al., Paris, France. In Eur J Med Genet, 2014
Duplication of paternally expressed genes MKRN3, MAGEL2 and NDN in two autistic patients without extra material of a neighboring region enhances their likelihood to be genes related to autism.
Necdin promotes ubiquitin-dependent degradation of PIAS1 SUMO E3 ligase.
Yoshikawa et al., Suita, Japan. In Plos One, 2013
Co-immunoprecipitation analysis revealed that necdin, MAGED1, MAGEF1 and MAGEL2 bound to PIAS1 but not to Nsmce2 or Cbx4.
Genome-wide mapping of loci explaining variance in scrotal circumference in Nellore cattle.
Garcia et al., Jaboticabal, Brazil. In Plos One, 2013
Based on intensive literature mining, SP4, MAGEL2, SH3RF2, PDE5A and SNAI2 are proposed as novel candidate genes for SC, as they affect growth and testicular size in other animal models.
Muscle transcriptomic investigation of late fetal development identifies candidate genes for piglet maturity.
Liaubet et al., France. In Bmc Genomics, 2013
Among these paternally regulated genes, some known imprinted genes, such as MAGEL2 or IGF2, were identified and could have a key role in the maturation process.
Truncating mutations of MAGEL2 cause Prader-Willi phenotypes and autism.
Yang et al., Houston, United States. In Nat Genet, 2013
We report four individuals with truncating mutations on the paternal allele of MAGEL2, a gene within the PWS domain.
Knockdown of CDKN1C (p57(kip2)) and PHLDA2 results in developmental changes in bovine pre-implantation embryos.
Khatib et al., Madison, United States. In Plos One, 2012
Expression levels of 18 imprinted genes (MAGEL2, UBE3A, IGF2R, NAP1L5, TSSC4, PEG3, NDN, CDKN1C, PHLDA2, MKRN3, USP29, NNAT, PEG10, RTL1, IGF2, H19, MIM1, and XIST) were compared between embryos reaching the blastocyst stage and growth-arrested embryos (degenerates) using quantitative real-time PCR (qRT-PCR).
Impaired hypothalamic regulation of endocrine function and delayed counterregulatory response to hypoglycemia in Magel2-null mice.
Wevrick et al., Edmonton, Canada. In Endocrinology, 2011
This study demonstrated that Magel2-null mice have abnormalities of hypothalamic endocrine axes that recapitulate phenotypes in Prader-Willi syndrome.
A single postnatal injection of oxytocin rescues the lethal feeding behaviour in mouse newborns deficient for the imprinted Magel2 gene.
Muscatelli et al., Marseille, France. In Hum Mol Genet, 2011
Magel2-deficient mouse with 50% neonatal mortality had an altered onset of suckling activity and subsequent impaired feeding.
Lack of association between MAGEL2 and schizophrenia and mood disorders in the Japanese population.
Iwata et al., Japan. In Neuromolecular Med, 2010
Results suggest that MAGEL2 may not play a role in the pathophysiology of schizophrenia and mood disorders in the Japanese population.
Regionally reduced brain volume, altered serotonin neurochemistry, and abnormal behavior in mice null for the circadian rhythm output gene Magel2.
Wevrick et al., Edmonton, Canada. In Am J Med Genet B Neuropsychiatr Genet, 2010
role of the circadian rhythm output gene Magel2 in brain structure and behavior
The imprinted gene Magel2 regulates normal circadian output.
Stewart et al., Frederick, United States. In Nat Genet, 2007
The robust rhythmicity of Magel2 expression in the SCN and the altered behavioral rhythmicity of null mice reveal Magel2 to be a clock-controlled circadian output gene whose disruption results in some of the phenotypes characteristic of PWS.
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