Exon resequencing of H3K9 methyltransferase complex genes, EHMT1, EHTM2 and WIZ, in Japanese autism subjects / Shabeesh BALAN in Molecular Autism, (October 2014)  

Public ISBD [article]  inMolecular Autism > (October 2014) . - p.1-9 Titre : Exon resequencing of H3K9 methyltransferase complex genes, EHMT1, EHTM2 and WIZ, in Japanese autism subjects Type de document : Texte imprimé et/ou numérique Auteurs : Shabeesh BALAN, Auteur ; Yoshimi IWAYAMA, Auteur ; Motoko MAEKAWA, Auteur ; Tomoko TOYOTA, Auteur ; Tetsuo OHNISHI, Auteur ; Manabu TOYOSHIMA, Auteur ; Chie SHIMAMOTO, Auteur ; Kayoko ESAKI, Auteur ; Kazuo YAMADA, Auteur ; Yasuhide IWATA, Auteur ; Katsuaki SUZUKI, Auteur ; Masayuki IDE, Auteur ; Motonori OTA, Auteur ; Satoshi FUKUCHI, Auteur ; Masatsugu TSUJII, Auteur ; Norio MORI, Auteur ; Yoichi SHINKAI, Auteur ; Takeo YOSHIKAWA, Auteur Article en page(s) : p.1-9 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Histone H3 methylation at lysine 9 (H3K9) is a conserved epigenetic signal, mediating heterochromatin formation by trimethylation, and transcriptional silencing by dimethylation. Defective GLP (Ehmt1) and G9a (Ehmt2) histone lysine methyltransferases, involved in mono and dimethylation of H3K9, confer autistic phenotypes and behavioral abnormalities in animal models. Moreover, EHMT1 loss of function results in Kleefstra syndrome, characterized by severe intellectual disability, developmental delays and psychiatric disorders. We examined the possible role of histone methyltransferases in the etiology of autism spectrum disorders (ASD) and suggest that rare functional variants in these genes that regulate H3K9 methylation may be associated with ASD. En ligne : http://dx.doi.org/10.1186/2040-2392-5-49 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=276 [article] Exon resequencing of H3K9 methyltransferase complex genes, EHMT1, EHTM2 and WIZ, in Japanese autism subjects [Texte imprimé et/ou numérique] / Shabeesh BALAN, Auteur ; Yoshimi IWAYAMA, Auteur ; Motoko MAEKAWA, Auteur ; Tomoko TOYOTA, Auteur ; Tetsuo OHNISHI, Auteur ; Manabu TOYOSHIMA, Auteur ; Chie SHIMAMOTO, Auteur ; Kayoko ESAKI, Auteur ; Kazuo YAMADA, Auteur ; Yasuhide IWATA, Auteur ; Katsuaki SUZUKI, Auteur ; Masayuki IDE, Auteur ; Motonori OTA, Auteur ; Satoshi FUKUCHI, Auteur ; Masatsugu TSUJII, Auteur ; Norio MORI, Auteur ; Yoichi SHINKAI, Auteur ; Takeo YOSHIKAWA, Auteur . - p.1-9. Langues : Anglais (eng) in Molecular Autism > (October 2014) . - p.1-9 Index. décimale : PER Périodiques Résumé : Histone H3 methylation at lysine 9 (H3K9) is a conserved epigenetic signal, mediating heterochromatin formation by trimethylation, and transcriptional silencing by dimethylation. Defective GLP (Ehmt1) and G9a (Ehmt2) histone lysine methyltransferases, involved in mono and dimethylation of H3K9, confer autistic phenotypes and behavioral abnormalities in animal models. Moreover, EHMT1 loss of function results in Kleefstra syndrome, characterized by severe intellectual disability, developmental delays and psychiatric disorders. We examined the possible role of histone methyltransferases in the etiology of autism spectrum disorders (ASD) and suggest that rare functional variants in these genes that regulate H3K9 methylation may be associated with ASD. En ligne : http://dx.doi.org/10.1186/2040-2392-5-49 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=276

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