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10.1016/j.vph.2020.106823 http://scihub22266oqcxt.onion/10.1016/j.vph.2020.106823 33232769!7680014!33232769     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       Vascul+Pharmacol 2021 ; 137 (ä): 106823 Nephropedia Template TP {{tp|p=33232769|t=2021. SARS-CoV-2 spike protein-mediated cell signaling in lung vascular cells |pdf=|usr=}}{{33232769}} gab.com Text SARS-CoV-2 spike protein-mediated cell signaling in lung vascular cells JO: Vascul Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=33232769 #FOAvip Currently, the world is suffering from the pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that uses angiotensin-converting enzyme 2 (ACE2) as a receptor to enter the host cells. So far, 60 million people have been infected with SARS-CoV-2, and 1.4 million people have died because of COVID-19 worldwide, causing serious health, economical, and sociological problems. However, the mechanism of the effect of SARS-CoV-2 on human host cells has not been defined. The present study reports that the SARS-CoV-2 spike protein alone without the rest of the viral components is sufficient to elicit cell signaling in lung vascular cells. The treatment of human pulmonary artery smooth muscle cells or human pulmonary artery endothelial cells with recombinant SARS-CoV-2 spike protein S1 subunit (Val16 - Gln690) at 10 ng/ml (0.13 nM) caused an activation of MEK phosphorylation. The activation kinetics was transient with a peak at 10 min. The recombinant protein that contains only the ACE2 receptor-binding domain of the SARS-CoV-2 spike protein S1 subunit (Arg319 - Phe541), on the other hand, did not cause this activation. Consistent with the activation of cell growth signaling in lung vascular cells by the SARS-CoV-2 spike protein, pulmonary vascular walls were found to be thickened in COVID-19 patients. Thus, SARS-CoV-2 spike protein-mediated cell growth signaling may participate in adverse cardiovascular/pulmonary outcomes, and this mechanism may provide new therapeutic targets to combat COVID-19. Twit Text FOAVip SARS-CoV-2 spike protein-mediated cell signaling in lung vascular cells ????Vascul Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=33232769 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33232769 #FOAvip English Wikipedia <ref>{{Cite pmid|33232769}}</ref> SARS-CoV-2 spike protein-mediated cell signaling in lung vascular cells #MMPMID33232769 Suzuki YJ; Nikolaienko SI; Dibrova VA; Dibrova YV; Vasylyk VM; Novikov MY; Shults NV; Gychka SG Vascul Pharmacol 2021[Apr]; 137 (ä): 106823 PMID33232769show ga Currently, the world is suffering from the pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that uses angiotensin-converting enzyme 2 (ACE2) as a receptor to enter the host cells. So far, 60 million people have been infected with SARS-CoV-2, and 1.4 million people have died because of COVID-19 worldwide, causing serious health, economical, and sociological problems. However, the mechanism of the effect of SARS-CoV-2 on human host cells has not been defined. The present study reports that the SARS-CoV-2 spike protein alone without the rest of the viral components is sufficient to elicit cell signaling in lung vascular cells. The treatment of human pulmonary artery smooth muscle cells or human pulmonary artery endothelial cells with recombinant SARS-CoV-2 spike protein S1 subunit (Val16 - Gln690) at 10 ng/ml (0.13 nM) caused an activation of MEK phosphorylation. The activation kinetics was transient with a peak at 10 min. The recombinant protein that contains only the ACE2 receptor-binding domain of the SARS-CoV-2 spike protein S1 subunit (Arg319 - Phe541), on the other hand, did not cause this activation. Consistent with the activation of cell growth signaling in lung vascular cells by the SARS-CoV-2 spike protein, pulmonary vascular walls were found to be thickened in COVID-19 patients. Thus, SARS-CoV-2 spike protein-mediated cell growth signaling may participate in adverse cardiovascular/pulmonary outcomes, and this mechanism may provide new therapeutic targets to combat COVID-19. |Angiotensin-Converting Enzyme 2/metabolism[MESH] |COVID-19/*metabolism/pathology/virology[MESH] |Cells, Cultured[MESH] |Endothelial Cells/*metabolism/pathology/virology[MESH] |Host-Pathogen Interactions[MESH] |Humans[MESH] |Kinetics[MESH] |Lung/*blood supply[MESH] |Mitogen-Activated Protein Kinase Kinases/metabolism[MESH] |Muscle, Smooth, Vascular/*metabolism/pathology/virology[MESH] |Myocytes, Smooth Muscle/*metabolism/pathology/virology[MESH] |Phosphorylation[MESH] |Protein Interaction Domains and Motifs[MESH] |Pulmonary Artery/metabolism/pathology/virology[MESH] |Receptors, Virus/metabolism[MESH] |SARS-CoV-2/*metabolism/pathogenicity[MESH] |Signal Transduction[MESH]SARS-CoV-2 spike protein-mediated cell signaling in lung vascular cell(epmc).pdf DeepDyve Pubget Overpricing