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10.1371/journal.pgen.1006031 http://scihub22266oqcxt.onion/10.1371/journal.pgen.1006031 C4859507!4859507 !27152426     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27152426 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 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\27152426 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+Genet 2016 ; 12 (5 ): e1006031 Nephropedia Template TP {{tp|p=27152426 |t=2016. PABPN1-Dependent mRNA Processing Induces Muscle Wasting |pdf=|usr=}}{{27152426 }} gab.com Text PABPN1-Dependent mRNA Processing Induces Muscle Wasting JO: PLoS Genet http://www.kidney.de/pget.php?&tw=1&pmid=27152426 #FOAvip Poly(A) Binding Protein Nuclear 1 (PABPN1) is a multifunctional regulator of mRNA processing, and its expression levels specifically decline in aging muscles. An expansion mutation in PABPN1 is the genetic cause of oculopharyngeal muscle dystrophy (OPMD), a late onset and rare myopathy. Moreover, reduced PABPN1 expression correlates with symptom manifestation in OPMD. PABPN1 regulates alternative polyadenylation site (PAS) utilization. However, the impact of PAS utilization on cell and tissue function is poorly understood. We hypothesized that altered PABPN1 expression levels is an underlying cause of muscle wasting. To test this, we stably down-regulated PABPN1 in mouse tibialis anterior (TA) muscles by localized injection of adeno-associated viruses expressing shRNA to PABPN1 (shPab). We found that a mild reduction in PABPN1 levels causes muscle pathology including myofiber atrophy, thickening of extracellular matrix and myofiber-type transition. Moreover, reduced PABPN1 levels caused a consistent decline in distal PAS utilization in the 3'-UTR of a subset of OPMD-dysregulated genes. This alternative PAS utilization led to up-regulation of Atrogin-1, a key muscle atrophy regulator, but down regulation of proteasomal genes. Additionally reduced PABPN1 levels caused a reduction in proteasomal activity, and transition in MyHC isotope expression pattern in myofibers. We suggest that PABPN1-mediated alternative PAS utilization plays a central role in aging-associated muscle wasting. Twit Text FOAVip PABPN1-Dependent mRNA Processing Induces Muscle Wasting ????PLoS Genet http://www.kidney.de/pget.php?&tw=1&pmid=27152426 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27152426 #FOAvip English Wikipedia <ref>{{Cite pmid|27152426 }}</ref> PABPN1-Dependent mRNA Processing Induces Muscle Wasting #MMPMID27152426 Riaz M ; Raz Y ; van Putten M ; Paniagua-Soriano G ; Krom YD ; Florea BI ; Raz V PLoS Genet 2016[May]; 12 (5 ): e1006031 PMID27152426 show ga Poly(A) Binding Protein Nuclear 1 (PABPN1) is a multifunctional regulator of mRNA processing, and its expression levels specifically decline in aging muscles. An expansion mutation in PABPN1 is the genetic cause of oculopharyngeal muscle dystrophy (OPMD), a late onset and rare myopathy. Moreover, reduced PABPN1 expression correlates with symptom manifestation in OPMD. PABPN1 regulates alternative polyadenylation site (PAS) utilization. However, the impact of PAS utilization on cell and tissue function is poorly understood. We hypothesized that altered PABPN1 expression levels is an underlying cause of muscle wasting. To test this, we stably down-regulated PABPN1 in mouse tibialis anterior (TA) muscles by localized injection of adeno-associated viruses expressing shRNA to PABPN1 (shPab). We found that a mild reduction in PABPN1 levels causes muscle pathology including myofiber atrophy, thickening of extracellular matrix and myofiber-type transition. Moreover, reduced PABPN1 levels caused a consistent decline in distal PAS utilization in the 3'-UTR of a subset of OPMD-dysregulated genes. This alternative PAS utilization led to up-regulation of Atrogin-1, a key muscle atrophy regulator, but down regulation of proteasomal genes. Additionally reduced PABPN1 levels caused a reduction in proteasomal activity, and transition in MyHC isotope expression pattern in myofibers. We suggest that PABPN1-mediated alternative PAS utilization plays a central role in aging-associated muscle wasting. |Aging/*genetics/pathology [MESH] |Animals [MESH] |Dependovirus/genetics [MESH] |Gene Expression Regulation [MESH] |Humans [MESH] |Mice [MESH] |Muscle Proteins/*biosynthesis/genetics [MESH] |Muscle, Skeletal/metabolism/pathology [MESH] |Muscular Dystrophy, Oculopharyngeal/*genetics/metabolism/pathology [MESH] |Poly(A)-Binding Protein I/biosynthesis/*genetics [MESH] |RNA, Messenger/biosynthesis [MESH]PABPN1-Dependent mRNA Processing Induces Muscle Wasting (epmc).pdf DeepDyve Pubget Overpricing