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10.1016/j.ajhg.2015.08.002 http://scihub22266oqcxt.onion/10.1016/j.ajhg.2015.08.002 C4564991!4564991!26340334     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Hum+Genet 2015 ; 97 (3): 445-56 Nephropedia Template TP {{tp|p=26340334|t=2015. Chromatin-Remodeling-Factor ARID1B Represses Wnt/?-Catenin Signaling |pdf=|usr=}}{{26340334}} gab.com Text Chromatin-Remodeling-Factor ARID1B Represses Wnt/ -Catenin Signaling JO: Am J Hum Genet http://www.kidney.de/pget.php?&tw=1&pmid=26340334 #FOAvip The link of chromatin remodeling to both neurodevelopment and cancer has recently been highlighted by the identification of mutations affecting BAF chromatin-remodeling components, such as ARID1B, in individuals with intellectual disability and cancer. However, the underlying molecular mechanism(s) remains unknown. Here, we show that ARID1B is a repressor of Wnt/?-catenin signaling. Through whole-transcriptome analysis, we find that in individuals with intellectual disability and ARID1B loss-of-function mutations, Wnt/?-catenin target genes are upregulated. Using cellular models of low and high Wnt/?-catenin activity, we demonstrate that knockdown of ARID1B activates Wnt/?-catenin target genes and Wnt/?-catenin-dependent transcriptional reporters in a ?-catenin-dependent manner. Reciprocally, forced expression of ARID1B inhibits Wnt/?-catenin signaling downstream of the ?-catenin destruction complex. Both endogenous and exogenous ARID1B associate with ?-catenin and repress Wnt/?-catenin-mediated transcription through the BAF core subunit BRG1. Accordingly, mutations in ARID1B leading to partial or complete deletion of its BRG1-binding domain, as is often observed in intellectual disability and cancers, compromise association with ?-catenin, and the resultant ARID1B mutant proteins fail to suppress Wnt/?-catenin signaling. Finally, knockdown of ARID1B in mouse neuroblastoma cells leads to neurite outgrowth through ?-catenin. The data suggest that aberrations in chromatin-remodeling factors, such as ARID1B, might contribute to neurodevelopmental abnormalities and cancer through deregulation of developmental and oncogenic pathways, such as the Wnt/?-catenin signaling pathway. Twit Text FOAVip Chromatin-Remodeling-Factor ARID1B Represses Wnt/ -Catenin Signaling ????Am J Hum Genet http://www.kidney.de/pget.php?&tw=1&pmid=26340334 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26340334 #FOAvip English Wikipedia <ref>{{Cite pmid|26340334}}</ref> Chromatin-Remodeling-Factor ARID1B Represses Wnt/?-Catenin Signaling #MMPMID26340334 Vasileiou G; Ekici A; Uebe S; Zweier C; Hoyer J; Engels H; Behrens J; Reis A; Hadjihannas M Am J Hum Genet 2015[Sep]; 97 (3): 445-56 PMID26340334show ga The link of chromatin remodeling to both neurodevelopment and cancer has recently been highlighted by the identification of mutations affecting BAF chromatin-remodeling components, such as ARID1B, in individuals with intellectual disability and cancer. However, the underlying molecular mechanism(s) remains unknown. Here, we show that ARID1B is a repressor of Wnt/?-catenin signaling. Through whole-transcriptome analysis, we find that in individuals with intellectual disability and ARID1B loss-of-function mutations, Wnt/?-catenin target genes are upregulated. Using cellular models of low and high Wnt/?-catenin activity, we demonstrate that knockdown of ARID1B activates Wnt/?-catenin target genes and Wnt/?-catenin-dependent transcriptional reporters in a ?-catenin-dependent manner. Reciprocally, forced expression of ARID1B inhibits Wnt/?-catenin signaling downstream of the ?-catenin destruction complex. Both endogenous and exogenous ARID1B associate with ?-catenin and repress Wnt/?-catenin-mediated transcription through the BAF core subunit BRG1. Accordingly, mutations in ARID1B leading to partial or complete deletion of its BRG1-binding domain, as is often observed in intellectual disability and cancers, compromise association with ?-catenin, and the resultant ARID1B mutant proteins fail to suppress Wnt/?-catenin signaling. Finally, knockdown of ARID1B in mouse neuroblastoma cells leads to neurite outgrowth through ?-catenin. The data suggest that aberrations in chromatin-remodeling factors, such as ARID1B, might contribute to neurodevelopmental abnormalities and cancer through deregulation of developmental and oncogenic pathways, such as the Wnt/?-catenin signaling pathway. äChromatin-Remodeling-Factor ARID1B Represses Wnt/?-Catenin Signaling (epmc).pdf DeepDyve Pubget Overpricing