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.

10.1080/00325481.2020.1855921 http://scihub22266oqcxt.onion/10.1080/00325481.2020.1855921 33245005!7784782!33245005     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       Postgrad+Med 2021 ; 133 (5): 489-507 Nephropedia Template TP {{tp|p=33245005|t=2021. JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy |pdf=|usr=}}{{33245005}} gab.com Text JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy JO: Postgrad Med http://www.kidney.de/pget.php?&tw=1&pmid=33245005 #FOAvip As the incidence of COVID-19 increases with time, more and more efforts are made to pave a way out for the therapeutic strategies to deal with the disease progression. Inflammation being a significant influencer in COVID-19 patients, it drives our focus onto the signaling cascades of the JAK/STAT pathway. JAK phosphorylation mediated by cytokine receptor activation leads to phosphorylation of STATs that translocate into the nucleus to translate for inflammatory mediators. The SARS-CoV-2 structural proteins like spike, nucleocapsid, membrane and envelope proteins along with the non- structural proteins 1-16 including proteases like 3CL (pro) and PL(pro) promote its entry and survival in hosts. The SARS-CoV-2 infection triggers inflammation via the JAK/STAT pathway leading to recruitment of pneumocytes, endothelial cells, macrophages, monocytes, lymphocytes, natural killer cells and dendritic cells progressing towards cytokine storm. This produces various inflammatory markers in the host that determine the disease severity. The JAK/STAT signaling also mediates immune responses via B cell and T cell differentiation.With an attempt to reduce excessive inflammation, JAK/STAT inhibitors like Ruxolitinib, Baricitinib, Tofacitinib have been employed that mediate its actions via suppressors of cytokine signaling, cytokine inducible SH2 containing protein, Protein inhibitor of activated STAT and protein tyrosine phosphatases. Even though they are implicated with multiple adverse effects, the regulatory authorities have supported its use, and numerous clinical trials are in progress to prove their safety and efficacy. On the contrary, the exact mechanism of JAK/STAT inhibition at molecular levels remains speculative for which further investigations are required. Twit Text FOAVip JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy ????Postgrad Med http://www.kidney.de/pget.php?&tw=1&pmid=33245005 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33245005 #FOAvip English Wikipedia <ref>{{Cite pmid|33245005}}</ref> JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy #MMPMID33245005 Satarker S; Tom AA; Shaji RA; Alosious A; Luvis M; Nampoothiri M Postgrad Med 2021[Jun]; 133 (5): 489-507 PMID33245005show ga As the incidence of COVID-19 increases with time, more and more efforts are made to pave a way out for the therapeutic strategies to deal with the disease progression. Inflammation being a significant influencer in COVID-19 patients, it drives our focus onto the signaling cascades of the JAK/STAT pathway. JAK phosphorylation mediated by cytokine receptor activation leads to phosphorylation of STATs that translocate into the nucleus to translate for inflammatory mediators. The SARS-CoV-2 structural proteins like spike, nucleocapsid, membrane and envelope proteins along with the non- structural proteins 1-16 including proteases like 3CL (pro) and PL(pro) promote its entry and survival in hosts. The SARS-CoV-2 infection triggers inflammation via the JAK/STAT pathway leading to recruitment of pneumocytes, endothelial cells, macrophages, monocytes, lymphocytes, natural killer cells and dendritic cells progressing towards cytokine storm. This produces various inflammatory markers in the host that determine the disease severity. The JAK/STAT signaling also mediates immune responses via B cell and T cell differentiation.With an attempt to reduce excessive inflammation, JAK/STAT inhibitors like Ruxolitinib, Baricitinib, Tofacitinib have been employed that mediate its actions via suppressors of cytokine signaling, cytokine inducible SH2 containing protein, Protein inhibitor of activated STAT and protein tyrosine phosphatases. Even though they are implicated with multiple adverse effects, the regulatory authorities have supported its use, and numerous clinical trials are in progress to prove their safety and efficacy. On the contrary, the exact mechanism of JAK/STAT inhibition at molecular levels remains speculative for which further investigations are required. |*COVID-19 Drug Treatment[MESH] |Anti-Inflammatory Agents/*therapeutic use[MESH] |COVID-19/metabolism[MESH] |Cytokines/metabolism[MESH] |Dose-Response Relationship, Drug[MESH] |Endothelial Cells/metabolism[MESH] |Gene Expression Regulation/drug effects[MESH] |Humans[MESH] |Inflammation Mediators/*metabolism[MESH] |Inflammation/*drug therapy/metabolism[MESH] |Janus Kinase Inhibitors/*therapeutic use[MESH]JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy(epmc).pdf DeepDyve Pubget Overpricing