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10.1172/jci.insight.148999 http://scihub22266oqcxt.onion/10.1172/jci.insight.148999 34291736!8410055!34291736     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight 2021 ; 6 (14): ä Nephropedia Template TP {{tp|p=34291736|t=2021. L-SIGN is a receptor on liver sinusoidal endothelial cells for SARS-CoV-2 virus |pdf=|usr=}}{{34291736}} gab.com Text L-SIGN is a receptor on liver sinusoidal endothelial cells for SARS-CoV-2 virus JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=34291736 #FOAvip Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains a pandemic. Severe disease is associated with dysfunction of multiple organs, but some infected cells do not express ACE2, the canonical entry receptor for SARS-CoV-2. Here, we report that the C-type lectin receptor L-SIGN interacted in a Ca2+-dependent manner with high-mannose-type N-glycans on the SARS-CoV-2 spike protein. We found that L-SIGN was highly expressed on human liver sinusoidal endothelial cells (LSECs) and lymph node lymphatic endothelial cells but not on blood endothelial cells. Using high-resolution confocal microscopy imaging, we detected SARS-CoV-2 viral proteins within the LSECs from liver autopsy samples from patients with COVID-19. We found that both pseudo-typed virus enveloped with SARS-CoV-2 spike protein and authentic SARS-CoV-2 virus infected L-SIGN-expressing cells relative to control cells. Moreover, blocking L-SIGN function reduced CoV-2-type infection. These results indicate that L-SIGN is a receptor for SARS-CoV-2 infection. LSECs are major sources of the clotting factors vWF and factor VIII (FVIII). LSECs from liver autopsy samples from patients with COVID-19 expressed substantially higher levels of vWF and FVIII than LSECs from uninfected liver samples. Our data demonstrate that L-SIGN is an endothelial cell receptor for SARS-CoV-2 that may contribute to COVID-19-associated coagulopathy. Twit Text FOAVip L-SIGN is a receptor on liver sinusoidal endothelial cells for SARS-CoV-2 virus ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=34291736 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34291736 #FOAvip English Wikipedia <ref>{{Cite pmid|34291736}}</ref> L-SIGN is a receptor on liver sinusoidal endothelial cells for SARS-CoV-2 virus #MMPMID34291736 Kondo Y; Larabee JL; Gao L; Shi H; Shao B; Hoover CM; McDaniel JM; Ho YC; Silasi-Mansat R; Archer-Hartmann SA; Azadi P; Srinivasan RS; Rezaie AR; Borczuk A; Laurence JC; Lupu F; Ahamed J; McEver RP; Papin JF; Yu Z; Xia L JCI Insight 2021[Jul]; 6 (14): ä PMID34291736show ga Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), remains a pandemic. Severe disease is associated with dysfunction of multiple organs, but some infected cells do not express ACE2, the canonical entry receptor for SARS-CoV-2. Here, we report that the C-type lectin receptor L-SIGN interacted in a Ca2+-dependent manner with high-mannose-type N-glycans on the SARS-CoV-2 spike protein. We found that L-SIGN was highly expressed on human liver sinusoidal endothelial cells (LSECs) and lymph node lymphatic endothelial cells but not on blood endothelial cells. Using high-resolution confocal microscopy imaging, we detected SARS-CoV-2 viral proteins within the LSECs from liver autopsy samples from patients with COVID-19. We found that both pseudo-typed virus enveloped with SARS-CoV-2 spike protein and authentic SARS-CoV-2 virus infected L-SIGN-expressing cells relative to control cells. Moreover, blocking L-SIGN function reduced CoV-2-type infection. These results indicate that L-SIGN is a receptor for SARS-CoV-2 infection. LSECs are major sources of the clotting factors vWF and factor VIII (FVIII). LSECs from liver autopsy samples from patients with COVID-19 expressed substantially higher levels of vWF and FVIII than LSECs from uninfected liver samples. Our data demonstrate that L-SIGN is an endothelial cell receptor for SARS-CoV-2 that may contribute to COVID-19-associated coagulopathy. |*COVID-19/metabolism/pathology/virology[MESH] |*Capillaries/metabolism/pathology/virology[MESH] |*Endothelial Cells/metabolism/pathology/virology[MESH] |*Lymphatic Vessels/metabolism/pathology/virology[MESH] |Cell Adhesion Molecules/*metabolism[MESH] |Gene Expression Profiling/methods[MESH] |Humans[MESH] |Lectins, C-Type/*metabolism[MESH] |Liver/*blood supply/pathology[MESH] |Receptors, Cell Surface/*metabolism[MESH] |SARS-CoV-2/*physiology[MESH] |Spike Glycoprotein, Coronavirus[MESH]L-SIGN is a receptor on liver sinusoidal endothelial cells for SARS-Co(epmc).pdf DeepDyve Pubget Overpricing