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10.3390/jcm5040039 http://scihub22266oqcxt.onion/10.3390/jcm5040039 C4850462!4850462 !27023622     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27023622 &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 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27023622 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Clin+Med 2016 ; 5 (4 ): ä Nephropedia Template TP {{tp|p=27023622 |t=2016. Osteopontin-A Master Regulator of Epithelial-Mesenchymal Transition |pdf=|usr=}}{{27023622 }} gab.com Text Osteopontin-A Master Regulator of Epithelial-Mesenchymal Transition JO: J Clin Med http://www.kidney.de/pget.php?&tw=1&pmid=27023622 #FOAvip Osteopontin (OPN) plays an important functional role in both physiologic and pathologic states. OPN is implicated in the progression of fibrosis, cancer, and metastatic disease in several organ systems. The epithelial-mesenchymal transition (EMT), first described in embryology, is increasingly being recognized as a significant contributor to fibrotic phenotypes and tumor progression. Several well-established transcription factors regulate EMT and are conserved across tissue types and organ systems, including TWIST, zinc finger E-box-binding homeobox (ZEB), and SNAIL-family members. Recent literature points to an important relationship between OPN and EMT, implicating OPN as a key regulatory component of EMT programs. In this review, OPN's interplay with traditional EMT activators, both directly and indirectly, will be discussed. Also, OPN's ability to restructure the tissue and tumor microenvironment to indirectly modify EMT will be reviewed. Together, these diverse pathways demonstrate that OPN is able to modulate EMT and provide new targets for directing therapeutics. Twit Text FOAVip Osteopontin-A Master Regulator of Epithelial-Mesenchymal Transition ????J Clin Med http://www.kidney.de/pget.php?&tw=1&pmid=27023622 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27023622 #FOAvip English Wikipedia <ref>{{Cite pmid|27023622 }}</ref> Osteopontin-A Master Regulator of Epithelial-Mesenchymal Transition #MMPMID27023622 Kothari AN ; Arffa ML ; Chang V ; Blackwell RH ; Syn WK ; Zhang J ; Mi Z ; Kuo PC J Clin Med 2016[Mar]; 5 (4 ): ä PMID27023622 show ga Osteopontin (OPN) plays an important functional role in both physiologic and pathologic states. OPN is implicated in the progression of fibrosis, cancer, and metastatic disease in several organ systems. The epithelial-mesenchymal transition (EMT), first described in embryology, is increasingly being recognized as a significant contributor to fibrotic phenotypes and tumor progression. Several well-established transcription factors regulate EMT and are conserved across tissue types and organ systems, including TWIST, zinc finger E-box-binding homeobox (ZEB), and SNAIL-family members. Recent literature points to an important relationship between OPN and EMT, implicating OPN as a key regulatory component of EMT programs. In this review, OPN's interplay with traditional EMT activators, both directly and indirectly, will be discussed. Also, OPN's ability to restructure the tissue and tumor microenvironment to indirectly modify EMT will be reviewed. Together, these diverse pathways demonstrate that OPN is able to modulate EMT and provide new targets for directing therapeutics. äOsteopontin-A Master Regulator of Epithelial-Mesenchymal Transition (epmc).pdf DeepDyve Pubget Overpricing