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10.1002/jmv.26743 http://scihub22266oqcxt.onion/10.1002/jmv.26743 33331649!9553089!33331649     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Med+Virol 2021 ; 93 (4): 2396-2405 Nephropedia Template TP {{tp|p=33331649|t=2021. Dysregulation of the mevalonate pathway during SARS-CoV-2 infection: An in silico study |pdf=|usr=}}{{33331649}} gab.com Text Dysregulation of the mevalonate pathway during SARS-CoV-2 infection: An in silico study JO: J Med Virol http://www.kidney.de/pget.php?&tw=1&pmid=33331649 #FOAvip SARS-CoV-2 triggers a dysregulated innate immune system activation. As the mevalonate pathway (MVP) prevents the activation of inflammasomes and cytokine release and regulates endosomal transport, compromised signaling could be associated with the pathobiology of COVID-19. Prior transcriptomic studies of host cells in response to SARS-CoV-2 infection have not reported to date the effects of SARS-CoV-2 on the MVP. In this study, we accessed public data sets to report in silico investigations into gene expression. In addition, we proposed candidate genes that are thought to have a direct association with the pathogenesis of COVID-19, and which may be dependent on signals derived from the MVP. Our results revealed dysregulation of genes involved in the MVP. These results were not found when investigating the gene expression data from host cells infected with H3N2 influenza virus, H1N1 influenza virus, or respiratory syncytial virus. Our manually curated gene set showed significant gene expression variability in A549 cells infected with SARS-CoV-2, as per Blanco-Melo et al. data set (GSE147507). In light of the present findings, SARS-CoV-2 could hijack the MVP, leading to hyperinflammatory responses. Prompt reconstitution of this pathway with available agents should be considered in future studies. Twit Text FOAVip Dysregulation of the mevalonate pathway during SARS-CoV-2 infection: An in silico study ????J Med Virol http://www.kidney.de/pget.php?&tw=1&pmid=33331649 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33331649 #FOAvip English Wikipedia <ref>{{Cite pmid|33331649}}</ref> Dysregulation of the mevalonate pathway during SARS-CoV-2 infection: An in silico study #MMPMID33331649 Gomez Marti JL; Wells A; Brufsky AM J Med Virol 2021[Apr]; 93 (4): 2396-2405 PMID33331649show ga SARS-CoV-2 triggers a dysregulated innate immune system activation. As the mevalonate pathway (MVP) prevents the activation of inflammasomes and cytokine release and regulates endosomal transport, compromised signaling could be associated with the pathobiology of COVID-19. Prior transcriptomic studies of host cells in response to SARS-CoV-2 infection have not reported to date the effects of SARS-CoV-2 on the MVP. In this study, we accessed public data sets to report in silico investigations into gene expression. In addition, we proposed candidate genes that are thought to have a direct association with the pathogenesis of COVID-19, and which may be dependent on signals derived from the MVP. Our results revealed dysregulation of genes involved in the MVP. These results were not found when investigating the gene expression data from host cells infected with H3N2 influenza virus, H1N1 influenza virus, or respiratory syncytial virus. Our manually curated gene set showed significant gene expression variability in A549 cells infected with SARS-CoV-2, as per Blanco-Melo et al. data set (GSE147507). In light of the present findings, SARS-CoV-2 could hijack the MVP, leading to hyperinflammatory responses. Prompt reconstitution of this pathway with available agents should be considered in future studies. |A549 Cells[MESH] |Autophagy[MESH] |COVID-19/genetics/immunology/*metabolism/virology[MESH] |Computer Simulation[MESH] |Cytokines/immunology/metabolism[MESH] |HMGB1 Protein/genetics/metabolism[MESH] |Host-Pathogen Interactions[MESH] |Humans[MESH] |Influenza A Virus, H1N1 Subtype/genetics/metabolism[MESH] |Influenza A Virus, H3N2 Subtype/genetics/metabolism[MESH] |Influenza, Human/immunology/metabolism[MESH] |Mevalonic Acid/*metabolism[MESH] |SAM Domain and HD Domain-Containing Protein 1/genetics/metabolism[MESH] |SARS-CoV-2/genetics/*metabolism[MESH] |Signal Transduction[MESH] |Transcriptome[MESH]Dysregulation of the mevalonate pathway during SARS-CoV-2 infection: A(epmc).pdf DeepDyve Pubget Overpricing