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10.4049/jimmunol.1600815 http://scihub22266oqcxt.onion/10.4049/jimmunol.1600815 C5011012!5011012!27489283     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 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\27489283.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Immunol 2016 ; 197 (6): 2280-9 Nephropedia Template TP {{tp|p=27489283|t=2016. Rpl22 Loss Selectively Impairs a? T Cell Development By Dysregulating ER Stress Signaling |pdf=|usr=}}{{27489283}} gab.com Text Rpl22 Loss Selectively Impairs a T Cell Development By Dysregulating ER Stress Signaling JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27489283 #FOAvip While ribosomal proteins (RP) are thought to primarily facilitate biogenesis of the ribosome and its ability to synthesize protein, emerging evidence suggests that individual RP can perform critical regulatory functions that control developmental processes. We showed previously that despite the ubiquitous expression of the RP, Rpl22, germline ablation of Rpl22 in mice causes a selective, p53-dependent block in the development of ??, but not ??, T cell progenitors. Nevertheless, the basis by which Rpl22 loss selectively induces p53 in ?? T cell progenitors remained unclear. We show here that Rpl22 regulates the development of ?? T cells by restraining endoplasmic reticulum (ER) stress responses. In the absence of Rpl22, ER stress is exacerbated in ??, but not ??, T cell progenitors. The exacerbated ER stress in Rpl22-deficient ?? T lineage progenitors is responsible for selective induction of p53 and their arrest, as pharmacological induction of stress is sufficient to induce p53 and replicate the selective block of ?? T cells, and attenuation of ER stress signaling by knockdown of PERK, an ER stress sensor, blunts p53 induction and rescues development of Rpl22-deficient ?? T cell progenitors. Rpl22-deficiency appears to exacerbate ER stress by interfering with the ability of ER stress signals to block new protein synthesis. Our finding that Rpl22-deficiency exacerbates ER stress responses and induces p53 in ?? T cell progenitors provides insight into how a ubiquitously expressed RP can perform regulatory functions that are selectively required by some cell lineages but not others. Twit Text FOAVip Rpl22 Loss Selectively Impairs a T Cell Development By Dysregulating ER Stress Signaling ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=27489283 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27489283 #FOAvip English Wikipedia <ref>{{Cite pmid|27489283}}</ref> Rpl22 Loss Selectively Impairs a? T Cell Development By Dysregulating ER Stress Signaling #MMPMID27489283 Solanki NR; Stadanlick JE; Zhang Y; Duc AC; Lee SY; Lauritsen JPH; Zhang Z; Wiest DL J Immunol 2016[Sep]; 197 (6): 2280-9 PMID27489283show ga While ribosomal proteins (RP) are thought to primarily facilitate biogenesis of the ribosome and its ability to synthesize protein, emerging evidence suggests that individual RP can perform critical regulatory functions that control developmental processes. We showed previously that despite the ubiquitous expression of the RP, Rpl22, germline ablation of Rpl22 in mice causes a selective, p53-dependent block in the development of ??, but not ??, T cell progenitors. Nevertheless, the basis by which Rpl22 loss selectively induces p53 in ?? T cell progenitors remained unclear. We show here that Rpl22 regulates the development of ?? T cells by restraining endoplasmic reticulum (ER) stress responses. In the absence of Rpl22, ER stress is exacerbated in ??, but not ??, T cell progenitors. The exacerbated ER stress in Rpl22-deficient ?? T lineage progenitors is responsible for selective induction of p53 and their arrest, as pharmacological induction of stress is sufficient to induce p53 and replicate the selective block of ?? T cells, and attenuation of ER stress signaling by knockdown of PERK, an ER stress sensor, blunts p53 induction and rescues development of Rpl22-deficient ?? T cell progenitors. Rpl22-deficiency appears to exacerbate ER stress by interfering with the ability of ER stress signals to block new protein synthesis. Our finding that Rpl22-deficiency exacerbates ER stress responses and induces p53 in ?? T cell progenitors provides insight into how a ubiquitously expressed RP can perform regulatory functions that are selectively required by some cell lineages but not others. äRpl22 Loss Selectively Impairs a? T Cell Development By Dysregulating (epmc).pdf DeepDyve Pubget Overpricing