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10.1016/j.molcel.2014.08.027 http://scihub22266oqcxt.onion/10.1016/j.molcel.2014.08.027 C4224598!4224598 !25263597     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 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 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 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25263597 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Cell 2014 ; 56 (2 ): 311-322 Nephropedia Template TP {{tp|p=25263597 |t=2014. Loss of MBNL leads to disruption of developmentally regulated alternative polyadenylation in RNA-mediated disease |pdf=|usr=}}{{25263597 }} gab.com Text Loss of MBNL leads to disruption of developmentally regulated alternative polyadenylation in RNA-mediated disease JO: Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=25263597 #FOAvip Inhibition of muscleblind-like (MBNL) activity due to sequestration by microsatellite expansion RNAs is a major pathogenic event in the RNA-mediated disease myotonic dystrophy (DM). Although MBNL1 and MBNL2 bind to nascent transcripts to regulate alternative splicing during muscle and brain development, another major binding site for the MBNL protein family is the 3' untranslated region of target RNAs. Here, we report that depletion of Mbnl proteins in mouse embryo fibroblasts leads to misregulation of thousands of alternative polyadenylation events. HITS-CLIP and minigene reporter analyses indicate that these polyadenylation switches are a direct consequence of MBNL binding to target RNAs. Misregulated alternative polyadenylation also occurs in skeletal muscle in a mouse polyCUG model and human DM, resulting in the persistence of neonatal polyadenylation patterns. These findings reveal an additional developmental function for MBNL proteins and demonstrate that DM is characterized by misregulation of pre-mRNA processing at multiple levels. Twit Text FOAVip Loss of MBNL leads to disruption of developmentally regulated alternative polyadenylation in RNA-mediated disease ????Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=25263597 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25263597 #FOAvip English Wikipedia <ref>{{Cite pmid|25263597 }}</ref> Loss of MBNL leads to disruption of developmentally regulated alternative polyadenylation in RNA-mediated disease #MMPMID25263597 Batra R ; Charizanis K ; Manchanda M ; Mohan A ; Li M ; Finn DJ ; Goodwin M ; Zhang C ; Sobczak K ; Thornton CA ; Swanson MS Mol Cell 2014[Oct]; 56 (2 ): 311-322 PMID25263597 show ga Inhibition of muscleblind-like (MBNL) activity due to sequestration by microsatellite expansion RNAs is a major pathogenic event in the RNA-mediated disease myotonic dystrophy (DM). Although MBNL1 and MBNL2 bind to nascent transcripts to regulate alternative splicing during muscle and brain development, another major binding site for the MBNL protein family is the 3' untranslated region of target RNAs. Here, we report that depletion of Mbnl proteins in mouse embryo fibroblasts leads to misregulation of thousands of alternative polyadenylation events. HITS-CLIP and minigene reporter analyses indicate that these polyadenylation switches are a direct consequence of MBNL binding to target RNAs. Misregulated alternative polyadenylation also occurs in skeletal muscle in a mouse polyCUG model and human DM, resulting in the persistence of neonatal polyadenylation patterns. These findings reveal an additional developmental function for MBNL proteins and demonstrate that DM is characterized by misregulation of pre-mRNA processing at multiple levels. |3' Untranslated Regions/genetics [MESH] |Alternative Splicing/*genetics [MESH] |Animals [MESH] |Binding Sites/genetics [MESH] |Carrier Proteins/*genetics/metabolism [MESH] |Cells, Cultured [MESH] |DNA-Binding Proteins/*genetics/metabolism [MESH] |Gene Expression Regulation, Developmental [MESH] |Humans [MESH] |Mice [MESH] |Microsatellite Repeats/genetics [MESH] |Muscle, Skeletal/cytology/metabolism [MESH] |Myotonic Dystrophy/genetics [MESH] |Polyadenylation/*genetics [MESH] |Protein Binding [MESH] |RNA Interference [MESH] |RNA Precursors/genetics [MESH] |RNA Processing, Post-Transcriptional/genetics [MESH] |RNA, Messenger/metabolism [MESH] |RNA, Small Interfering [MESH]Loss of MBNL leads to disruption of developmentally regulated alternat(epmc).pdf DeepDyve Pubget Overpricing