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10.1111/cas.13133 http://scihub22266oqcxt.onion/10.1111/cas.13133 C5329144!5329144!27987332     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27987332&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 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Sci 2017 ; 108 (2): 208-15 Nephropedia Template TP {{tp|p=27987332|t=2017. Neddylated Cullin 3 is required for vascular endothelial?cadherin?mediated endothelial barrier function |pdf=|usr=}}{{27987332}} gab.com Text Neddylated Cullin 3 is required for vascular endothelial cadherin mediated endothelial barrier function JO: Cancer Sci http://www.kidney.de/pget.php?&tw=1&pmid=27987332 #FOAvip Vascular endothelial (VE)?cadherin, a major endothelial adhesion molecule, regulates vascular permeability, and increased vascular permeability has been observed in several cancers. The aim of this study was to elucidate the role of the NEDD8?Cullin E3 ligase, in maintaining barrier permeability. To this end, we investigated the effects of the inhibition of Cullin E3 ligases, by using inhibitors and knockdown techniques in HUVECs. Furthermore, we analyzed the mRNA and protein levels of the ligases by quantitative RT?PCR and Western blotting, respectively. The results revealed that NEDD8?conjugated Cullin 3 is required for VE?cadherin?mediated endothelial barrier functions. Treatment of HUVECs with MLN4924, a chemical inhibitor of the NEDD8?activating enzyme, led to high vascular permeability due to impaired cell?cell contact. Similar results were obtained when HUVECs were treated with siRNA directed against Cullin 3, one of the target substrates of NEDD8. Immunocytochemical staining showed that both treatments equally depleted VE?cadherin protein localized at the cell?cell borders. However, quantitative RT?PCR showed that there was no significant difference in the VE?cadherin mRNA levels between the treatment and control groups. In addition, cycloheximide chase assay revealed that the half?life of VE?cadherin protein was dramatically reduced by Cullin 3 depletion. Together, these findings suggest that neddylated Cullin 3 plays a crucial role in endothelial cell barrier function by regulating VE?cadherin. Twit Text FOAVip Neddylated Cullin 3 is required for vascular endothelial cadherin mediated endothelial barrier function ????Cancer Sci http://www.kidney.de/pget.php?&tw=1&pmid=27987332 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27987332 #FOAvip English Wikipedia <ref>{{Cite pmid|27987332}}</ref> Neddylated Cullin 3 is required for vascular endothelial?cadherin?mediated endothelial barrier function #MMPMID27987332 Sakaue T; Fujisaki A; Nakayama H; Maekawa M; Hiyoshi H; Kubota E; Joh T; Izutani H; Higashiyama S Cancer Sci 2017[Feb]; 108 (2): 208-15 PMID27987332show ga Vascular endothelial (VE)?cadherin, a major endothelial adhesion molecule, regulates vascular permeability, and increased vascular permeability has been observed in several cancers. The aim of this study was to elucidate the role of the NEDD8?Cullin E3 ligase, in maintaining barrier permeability. To this end, we investigated the effects of the inhibition of Cullin E3 ligases, by using inhibitors and knockdown techniques in HUVECs. Furthermore, we analyzed the mRNA and protein levels of the ligases by quantitative RT?PCR and Western blotting, respectively. The results revealed that NEDD8?conjugated Cullin 3 is required for VE?cadherin?mediated endothelial barrier functions. Treatment of HUVECs with MLN4924, a chemical inhibitor of the NEDD8?activating enzyme, led to high vascular permeability due to impaired cell?cell contact. Similar results were obtained when HUVECs were treated with siRNA directed against Cullin 3, one of the target substrates of NEDD8. Immunocytochemical staining showed that both treatments equally depleted VE?cadherin protein localized at the cell?cell borders. However, quantitative RT?PCR showed that there was no significant difference in the VE?cadherin mRNA levels between the treatment and control groups. In addition, cycloheximide chase assay revealed that the half?life of VE?cadherin protein was dramatically reduced by Cullin 3 depletion. Together, these findings suggest that neddylated Cullin 3 plays a crucial role in endothelial cell barrier function by regulating VE?cadherin. äNeddylated Cullin 3 is required for vascular endothelial?cadherin?medi(epmc).pdf DeepDyve Pubget Overpricing