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10.1038/s41392-020-00292-7 http://scihub22266oqcxt.onion/10.1038/s41392-020-00292-7 32883951!7471497!32883951     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Signal+Transduct+Target+Ther 2020 ; 5 (1): 186 Nephropedia Template TP {{tp|p=32883951|t=2020. COVID-19-activated SREBP2 disturbs cholesterol biosynthesis and leads to cytokine storm |pdf=|usr=}}{{32883951}} gab.com Text COVID-19-activated SREBP2 disturbs cholesterol biosynthesis and leads to cytokine storm JO: Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=32883951 #FOAvip Sterol regulatory element binding protein-2 (SREBP-2) is activated by cytokines or pathogen, such as virus or bacteria, but its association with diminished cholesterol levels in COVID-19 patients is unknown. Here, we evaluated SREBP-2 activation in peripheral blood mononuclear cells of COVID-19 patients and verified the function of SREBP-2 in COVID-19. Intriguingly, we report the first observation of SREBP-2 C-terminal fragment in COVID-19 patients' blood and propose SREBP-2 C-terminal fragment as an indicator for determining severity. We confirmed that SREBP-2-induced cholesterol biosynthesis was suppressed by Sestrin-1 and PCSK9 expression, while the SREBP-2-induced inflammatory responses was upregulated in COVID-19 ICU patients. Using an infectious disease mouse model, inhibitors of SREBP-2 and NF-kappaB suppressed cytokine storms caused by viral infection and prevented pulmonary damages. These results collectively suggest that SREBP-2 can serve as an indicator for severity diagnosis and therapeutic target for preventing cytokine storm and lung damage in severe COVID-19 patients. Twit Text FOAVip COVID-19-activated SREBP2 disturbs cholesterol biosynthesis and leads to cytokine storm ????Signal Transduct Target Ther http://www.kidney.de/pget.php?&tw=1&pmid=32883951 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32883951 #FOAvip English Wikipedia <ref>{{Cite pmid|32883951}}</ref> COVID-19-activated SREBP2 disturbs cholesterol biosynthesis and leads to cytokine storm #MMPMID32883951 Lee W; Ahn JH; Park HH; Kim HN; Kim H; Yoo Y; Shin H; Hong KS; Jang JG; Park CG; Choi EY; Bae JS; Seo YK Signal Transduct Target Ther 2020[Sep]; 5 (1): 186 PMID32883951show ga Sterol regulatory element binding protein-2 (SREBP-2) is activated by cytokines or pathogen, such as virus or bacteria, but its association with diminished cholesterol levels in COVID-19 patients is unknown. Here, we evaluated SREBP-2 activation in peripheral blood mononuclear cells of COVID-19 patients and verified the function of SREBP-2 in COVID-19. Intriguingly, we report the first observation of SREBP-2 C-terminal fragment in COVID-19 patients' blood and propose SREBP-2 C-terminal fragment as an indicator for determining severity. We confirmed that SREBP-2-induced cholesterol biosynthesis was suppressed by Sestrin-1 and PCSK9 expression, while the SREBP-2-induced inflammatory responses was upregulated in COVID-19 ICU patients. Using an infectious disease mouse model, inhibitors of SREBP-2 and NF-kappaB suppressed cytokine storms caused by viral infection and prevented pulmonary damages. These results collectively suggest that SREBP-2 can serve as an indicator for severity diagnosis and therapeutic target for preventing cytokine storm and lung damage in severe COVID-19 patients. |Betacoronavirus/immunology/*pathogenicity[MESH] |COVID-19[MESH] |Case-Control Studies[MESH] |Cholesterol/*biosynthesis[MESH] |Coronavirus Infections/*genetics/immunology/mortality/virology[MESH] |Cytokine Release Syndrome/*genetics/immunology/mortality/virology[MESH] |Gene Expression Regulation[MESH] |Heat-Shock Proteins/genetics/immunology[MESH] |Host-Pathogen Interactions/*genetics/immunology[MESH] |Humans[MESH] |Intensive Care Units[MESH] |Interleukin-1beta/genetics/immunology[MESH] |L-Lactate Dehydrogenase/genetics/immunology[MESH] |Leukocytes, Mononuclear/*immunology/metabolism/virology[MESH] |Lung/immunology/metabolism/virology[MESH] |NF-kappa B/genetics/immunology[MESH] |Pandemics[MESH] |Pneumonia, Viral/*genetics/immunology/mortality/virology[MESH] |Primary Cell Culture[MESH] |Proprotein Convertase 9/genetics/immunology[MESH] |SARS-CoV-2[MESH] |Signal Transduction[MESH] |Sterol Regulatory Element Binding Protein 2/*genetics/immunology[MESH] |Survival Analysis[MESH]COVID-19-activated SREBP2 disturbs cholesterol biosynthesis and leads (epmc).pdf DeepDyve Pubget Overpricing