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10.1172/JCI143632 http://scihub22266oqcxt.onion/10.1172/JCI143632 34060486!8159689!34060486     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\34060486.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Clin+Invest 2021 ; 131 (11): ä Nephropedia Template TP {{tp|p=34060486|t=2021. Histone deficiency and accelerated replication stress in T cell aging |pdf=|usr=}}{{34060486}} gab.com Text Histone deficiency and accelerated replication stress in T cell aging JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=34060486 #FOAvip With increasing age, individuals are more vulnerable to viral infections such as with influenza or the SARS-CoV-2 virus. One age-associated defect in human T cells is the reduced expression of miR-181a. miR-181ab1 deficiency in peripheral murine T cells causes delayed viral clearance after infection, resembling human immune aging. Here we show that naive T cells from older individuals as well as miR-181ab1-deficient murine T cells develop excessive replication stress after activation, due to reduced histone expression and delayed S-phase cell cycle progression. Reduced histone expression was caused by the miR-181a target SIRT1 that directly repressed transcription of histone genes by binding to their promoters and reducing histone acetylation. Inhibition of SIRT1 activity or SIRT1 silencing increased histone expression, restored cell cycle progression, diminished the replication-stress response, and reduced the production of inflammatory mediators in replicating T cells from old individuals. Correspondingly, treatment with SIRT1 inhibitors improved viral clearance in mice with miR-181a-deficient T cells after LCMV infection. In conclusion, SIRT1 inhibition may be beneficial to treat systemic viral infection in older individuals by targeting antigen-specific T cells that develop replication stress due to miR-181a deficiency. Twit Text FOAVip Histone deficiency and accelerated replication stress in T cell aging ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=34060486 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34060486 #FOAvip English Wikipedia <ref>{{Cite pmid|34060486}}</ref> Histone deficiency and accelerated replication stress in T cell aging #MMPMID34060486 Kim C; Jin J; Ye Z; Jadhav RR; Gustafson CE; Hu B; Cao W; Tian L; Weyand CM; Goronzy JJ J Clin Invest 2021[Jun]; 131 (11): ä PMID34060486show ga With increasing age, individuals are more vulnerable to viral infections such as with influenza or the SARS-CoV-2 virus. One age-associated defect in human T cells is the reduced expression of miR-181a. miR-181ab1 deficiency in peripheral murine T cells causes delayed viral clearance after infection, resembling human immune aging. Here we show that naive T cells from older individuals as well as miR-181ab1-deficient murine T cells develop excessive replication stress after activation, due to reduced histone expression and delayed S-phase cell cycle progression. Reduced histone expression was caused by the miR-181a target SIRT1 that directly repressed transcription of histone genes by binding to their promoters and reducing histone acetylation. Inhibition of SIRT1 activity or SIRT1 silencing increased histone expression, restored cell cycle progression, diminished the replication-stress response, and reduced the production of inflammatory mediators in replicating T cells from old individuals. Correspondingly, treatment with SIRT1 inhibitors improved viral clearance in mice with miR-181a-deficient T cells after LCMV infection. In conclusion, SIRT1 inhibition may be beneficial to treat systemic viral infection in older individuals by targeting antigen-specific T cells that develop replication stress due to miR-181a deficiency. |Animals[MESH] |COVID-19/genetics/*immunology[MESH] |Cellular Senescence/genetics/*immunology[MESH] |Female[MESH] |Histones/*deficiency/immunology[MESH] |Humans[MESH] |Male[MESH] |Mice[MESH] |Mice, Knockout[MESH] |MicroRNAs/genetics/*immunology[MESH] |SARS-CoV-2/genetics/*immunology[MESH] |Sirtuin 1/genetics/immunology[MESH]Histone deficiency and accelerated replication stress in T cell aging (epmc).pdf DeepDyve Pubget Overpricing