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10.1080/19336918.2016.1170258 http://scihub22266oqcxt.onion/10.1080/19336918.2016.1170258 C4951171!4951171!27070187     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27070187&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 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Adh+Migr 2016 ; 10 (3): 310-21 Nephropedia Template TP {{tp|p=27070187|t=2016. Epithelial-mesenchymal transition during extravillous trophoblast differentiation |pdf=|usr=}}{{27070187}} gab.com Text Epithelial-mesenchymal transition during extravillous trophoblast differentiation JO: Cell Adh Migr http://www.kidney.de/pget.php?&tw=1&pmid=27070187 #FOAvip A successful pregnancy depends on the intricate and timely interactions of maternal and fetal cells. Placental extravillous cytotrophoblast invasion involves a cellular transition from an epithelial to mesenchymal phenotype. Villous cytotrophoblasts undergo a partial epithelial to mesenchymal transition (EMT) when differentiating into extravillous cytotrophoblasts and gain the capacity to migrate and invade. This review summarizes our current knowledge regarding known regulators of EMT in the human placenta, including the inducers of EMT, upstream transcription factors that control EMT and the downstream effectors, cell adhesion molecules and their differential expression and functions in pregnancy pathologies, preeclampsia (PE) and fetal growth restriction (FGR). The review also describes the research strategies that were used for the identification of the functional role of EMT targets in vitro. A better understanding of molecular pathways driven by placental EMT and further elucidation of signaling pathways underlying the developmental programs may offer novel strategies of targeted therapy for improving feto-placental growth in placental pathologies including PE and FGR. Twit Text FOAVip Epithelial-mesenchymal transition during extravillous trophoblast differentiation ????Cell Adh Migr http://www.kidney.de/pget.php?&tw=1&pmid=27070187 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27070187 #FOAvip English Wikipedia <ref>{{Cite pmid|27070187}}</ref> Epithelial-mesenchymal transition during extravillous trophoblast differentiation #MMPMID27070187 E. Davies J; Pollheimer J; Yong HEJ; Kokkinos MI; Kalionis B; Knöfler M; Murthi P Cell Adh Migr 2016[May]; 10 (3): 310-21 PMID27070187show ga A successful pregnancy depends on the intricate and timely interactions of maternal and fetal cells. Placental extravillous cytotrophoblast invasion involves a cellular transition from an epithelial to mesenchymal phenotype. Villous cytotrophoblasts undergo a partial epithelial to mesenchymal transition (EMT) when differentiating into extravillous cytotrophoblasts and gain the capacity to migrate and invade. This review summarizes our current knowledge regarding known regulators of EMT in the human placenta, including the inducers of EMT, upstream transcription factors that control EMT and the downstream effectors, cell adhesion molecules and their differential expression and functions in pregnancy pathologies, preeclampsia (PE) and fetal growth restriction (FGR). The review also describes the research strategies that were used for the identification of the functional role of EMT targets in vitro. A better understanding of molecular pathways driven by placental EMT and further elucidation of signaling pathways underlying the developmental programs may offer novel strategies of targeted therapy for improving feto-placental growth in placental pathologies including PE and FGR. äEpithelial-mesenchymal transition during extravillous trophoblast diff(epmc).pdf DeepDyve Pubget Overpricing