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10.1042/BJ20150821 http://scihub22266oqcxt.onion/10.1042/BJ20150821 C4867233!4867233!26542979     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Biochem+J 2016 ; 473 (3): 245-56 Nephropedia Template TP {{tp|p=26542979|t=2016. miR-1343 attenuates pathways of fibrosis by targeting the TGF-? receptors |pdf=|usr=}}{{26542979}} gab.com Text miR-1343 attenuates pathways of fibrosis by targeting the TGF- receptors JO: Biochem J http://www.kidney.de/pget.php?&tw=1&pmid=26542979 #FOAvip Irreversible respiratory obstruction resulting from progressive airway damage, inflammation and fibrosis is a feature of several chronic respiratory diseases, including cystic fibrosis (CF), idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). The cytokine transforming growth factor ? (TGF-?) has a pivotal role in promoting lung fibrosis and is implicated in respiratory disease severity. In the present study, we show that a previously uncharacterized miRNA, miR-1343, reduces the expression of both TGF-? receptor 1 and 2 by directly targeting their 3?-UTRs. After TGF-? exposure, elevated intracellular miR-1343 significantly decreases levels of activated TGF-? effector molecules, pSMAD2 (phosphorylated SMAD2) and pSMAD3 (phosphorylated SMAD3), when compared with a non-targeting control miRNA. As a result, the abundance of fibrotic markers is reduced, cell migration into a scratch wound impaired and epithelial-to-mesenchymal transition (EMT) repressed. Mature miR-1343 is readily detected in human neutrophils and HL-60 cells and is activated in response to stress in A549 lung epithelial cells. miR-1343 may have direct therapeutic applications in fibrotic lung disease. Twit Text FOAVip miR-1343 attenuates pathways of fibrosis by targeting the TGF- receptors ????Biochem J http://www.kidney.de/pget.php?&tw=1&pmid=26542979 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26542979 #FOAvip English Wikipedia <ref>{{Cite pmid|26542979}}</ref> miR-1343 attenuates pathways of fibrosis by targeting the TGF-? receptors #MMPMID26542979 Stolzenburg LR; Wachtel S; Dang H; Harris A Biochem J 2016[Feb]; 473 (3): 245-56 PMID26542979show ga Irreversible respiratory obstruction resulting from progressive airway damage, inflammation and fibrosis is a feature of several chronic respiratory diseases, including cystic fibrosis (CF), idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). The cytokine transforming growth factor ? (TGF-?) has a pivotal role in promoting lung fibrosis and is implicated in respiratory disease severity. In the present study, we show that a previously uncharacterized miRNA, miR-1343, reduces the expression of both TGF-? receptor 1 and 2 by directly targeting their 3?-UTRs. After TGF-? exposure, elevated intracellular miR-1343 significantly decreases levels of activated TGF-? effector molecules, pSMAD2 (phosphorylated SMAD2) and pSMAD3 (phosphorylated SMAD3), when compared with a non-targeting control miRNA. As a result, the abundance of fibrotic markers is reduced, cell migration into a scratch wound impaired and epithelial-to-mesenchymal transition (EMT) repressed. Mature miR-1343 is readily detected in human neutrophils and HL-60 cells and is activated in response to stress in A549 lung epithelial cells. miR-1343 may have direct therapeutic applications in fibrotic lung disease. ämiR-1343 attenuates pathways of fibrosis by targeting the TGF-? recept(epmc).pdf DeepDyve Pubget Overpricing