Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.7554/eLife.58603 http://scihub22266oqcxt.onion/10.7554/eLife.58603 32452762!7343387!32452762     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Elife 2020 ; 9 (ä): ä Nephropedia Template TP {{tp|p=32452762|t=2020. SARS-CoV-2 strategically mimics proteolytic activation of human ENaC |pdf=|usr=}}{{32452762}} gab.com Text SARS-CoV-2 strategically mimics proteolytic activation of human ENaC JO: Elife http://www.kidney.de/pget.php?&tw=1&pmid=32452762 #FOAvip Molecular mimicry is an evolutionary strategy adopted by viruses to exploit the host cellular machinery. We report that SARS-CoV-2 has evolved a unique S1/S2 cleavage site, absent in any previous coronavirus sequenced, resulting in the striking mimicry of an identical FURIN-cleavable peptide on the human epithelial sodium channel alpha-subunit (ENaC-alpha). Genetic alteration of ENaC-alpha causes aldosterone dysregulation in patients, highlighting that the FURIN site is critical for activation of ENaC. Single cell RNA-seq from 66 studies shows significant overlap between expression of ENaC-alpha and the viral receptor ACE2 in cell types linked to the cardiovascular-renal-pulmonary pathophysiology of COVID-19. Triangulating this cellular characterization with cleavage signatures of 178 proteases highlights proteolytic degeneracy wired into the SARS-CoV-2 lifecycle. Evolution of SARS-CoV-2 into a global pandemic may be driven in part by its targeted mimicry of ENaC-alpha, a protein critical for the homeostasis of airway surface liquid, whose misregulation is associated with respiratory conditions. Twit Text FOAVip SARS-CoV-2 strategically mimics proteolytic activation of human ENaC ????Elife http://www.kidney.de/pget.php?&tw=1&pmid=32452762 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32452762 #FOAvip English Wikipedia <ref>{{Cite pmid|32452762}}</ref> SARS-CoV-2 strategically mimics proteolytic activation of human ENaC #MMPMID32452762 Anand P; Puranik A; Aravamudan M; Venkatakrishnan AJ; Soundararajan V Elife 2020[May]; 9 (ä): ä PMID32452762show ga Molecular mimicry is an evolutionary strategy adopted by viruses to exploit the host cellular machinery. We report that SARS-CoV-2 has evolved a unique S1/S2 cleavage site, absent in any previous coronavirus sequenced, resulting in the striking mimicry of an identical FURIN-cleavable peptide on the human epithelial sodium channel alpha-subunit (ENaC-alpha). Genetic alteration of ENaC-alpha causes aldosterone dysregulation in patients, highlighting that the FURIN site is critical for activation of ENaC. Single cell RNA-seq from 66 studies shows significant overlap between expression of ENaC-alpha and the viral receptor ACE2 in cell types linked to the cardiovascular-renal-pulmonary pathophysiology of COVID-19. Triangulating this cellular characterization with cleavage signatures of 178 proteases highlights proteolytic degeneracy wired into the SARS-CoV-2 lifecycle. Evolution of SARS-CoV-2 into a global pandemic may be driven in part by its targeted mimicry of ENaC-alpha, a protein critical for the homeostasis of airway surface liquid, whose misregulation is associated with respiratory conditions. |*Molecular Mimicry[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Betacoronavirus/genetics/*metabolism/pathogenicity[MESH] |COVID-19[MESH] |Coronavirus Infections/*virology[MESH] |Epithelial Sodium Channels/genetics/*metabolism[MESH] |Host-Pathogen Interactions[MESH] |Humans[MESH] |Pandemics[MESH] |Peptide Hydrolases/*metabolism[MESH] |Peptidyl-Dipeptidase A/genetics/metabolism[MESH] |Pneumonia, Viral/*virology[MESH] |Proteolysis[MESH] |SARS-CoV-2[MESH] |Substrate Specificity[MESH] |Viral Envelope Proteins/genetics/*metabolism[MESH]SARS-CoV-2 strategically mimics proteolytic activation of human ENaC (epmc).pdf DeepDyve Pubget Overpricing