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10.1007/s12079-017-0426-2 http://scihub22266oqcxt.onion/10.1007/s12079-017-0426-2 C5842189!5842189 !29080087     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29080087 &cmd=llinks): Failed to open stream: HTTP request failed! 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The role of the endoplasmic reticulum protein calreticulin in mediating TGF-?-stimulated extracellular matrix production in fibrotic disease |pdf=|usr=}}{{29080087 }} gab.com Text The role of the endoplasmic reticulum protein calreticulin in mediating TGF- -stimulated extracellular matrix production in fibrotic disease JO: J Cell Commun Signal http://www.kidney.de/pget.php?&tw=1&pmid=29080087 #FOAvip Endoplasmic reticulum (ER) stress is a key factor contributing to fibrotic disease. Although ER stress is a short-term adaptive response, with chronic stimulation, it can activate pathways leading to fibrosis. ER stress can induce TGF-? signaling, a central driver of extracellular matrix production in fibrosis. This review will discuss the role of an ER protein, calreticulin (CRT), which has both chaperone and calcium regulatory functions, in fibrosis. CRT expression is upregulated in multiple different fibrotic diseases. The roles of CRT in regulation of fibronectin extracellular matrix assembly, extracellular matrix transcription, and collagen secretion and processing into the extracellular matrix will be discussed. Evidence for the importance of CRT in ER calcium release and NFAT activation downstream of TGF-? signaling will be presented. Finally, we will summarize evidence from animal models in which CRT expression is genetically reduced or experimentally downregulated in targeted tissues of adult animals and discuss how these models define a key role for CRT in fibrotic diseases. Twit Text FOAVip The role of the endoplasmic reticulum protein calreticulin in mediating TGF- -stimulated extracellular matrix production in fibrotic disease ????J Cell Commun Signal http://www.kidney.de/pget.php?&tw=1&pmid=29080087 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29080087 #FOAvip English Wikipedia <ref>{{Cite pmid|29080087 }}</ref> The role of the endoplasmic reticulum protein calreticulin in mediating TGF-?-stimulated extracellular matrix production in fibrotic disease #MMPMID29080087 Owusu BY ; Zimmerman KA ; Murphy-Ullrich JE J Cell Commun Signal 2018[Mar]; 12 (1 ): 289-299 PMID29080087 show ga Endoplasmic reticulum (ER) stress is a key factor contributing to fibrotic disease. Although ER stress is a short-term adaptive response, with chronic stimulation, it can activate pathways leading to fibrosis. ER stress can induce TGF-? signaling, a central driver of extracellular matrix production in fibrosis. This review will discuss the role of an ER protein, calreticulin (CRT), which has both chaperone and calcium regulatory functions, in fibrosis. CRT expression is upregulated in multiple different fibrotic diseases. The roles of CRT in regulation of fibronectin extracellular matrix assembly, extracellular matrix transcription, and collagen secretion and processing into the extracellular matrix will be discussed. Evidence for the importance of CRT in ER calcium release and NFAT activation downstream of TGF-? signaling will be presented. Finally, we will summarize evidence from animal models in which CRT expression is genetically reduced or experimentally downregulated in targeted tissues of adult animals and discuss how these models define a key role for CRT in fibrotic diseases. äThe role of the endoplasmic reticulum protein calreticulin in mediatin(epmc).pdf DeepDyve Pubget Overpricing