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10.1371/journal.ppat.1005842 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1005842 C5004865!5004865 !27575707     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 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\27575707 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+Pathog 2016 ; 12 (8 ): e1005842 Nephropedia Template TP {{tp|p=27575707 |t=2016. An Essential Viral Transcription Activator Modulates Chromatin Dynamics |pdf=|usr=}}{{27575707 }} gab.com Text An Essential Viral Transcription Activator Modulates Chromatin Dynamics JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=27575707 #FOAvip Although ICP4 is the only essential transcription activator of herpes simplex virus 1 (HSV-1), its mechanisms of action are still only partially understood. We and others propose a model in which HSV-1 genomes are chromatinized as a cellular defense to inhibit HSV-1 transcription. To counteract silencing, HSV-1 would have evolved proteins that prevent or destabilize chromatinization to activate transcription. These proteins should act as HSV-1 transcription activators. We have shown that HSV-1 genomes are organized in highly dynamic nucleosomes and that histone dynamics increase in cells infected with wild type HSV-1. We now show that whereas HSV-1 mutants encoding no functional ICP0 or VP16 partially enhanced histone dynamics, mutants encoding no functional ICP4 did so only minimally. Transient expression of ICP4 was sufficient to enhance histone dynamics in the absence of other HSV-1 proteins or HSV-1 DNA. The dynamics of H3.1 were increased in cells expressing ICP4 to a greater extent than those of H3.3. The dynamics of H2B were increased in cells expressing ICP4, whereas those of canonical H2A were not. ICP4 preferentially targets silencing H3.1 and may also target the silencing H2A variants. In infected cells, histone dynamics were increased in the viral replication compartments, where ICP4 localizes. These results suggest a mechanism whereby ICP4 activates transcription by disrupting, or preventing the formation of, stable silencing nucleosomes on HSV-1 genomes. Twit Text FOAVip An Essential Viral Transcription Activator Modulates Chromatin Dynamics ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=27575707 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27575707 #FOAvip English Wikipedia <ref>{{Cite pmid|27575707 }}</ref> An Essential Viral Transcription Activator Modulates Chromatin Dynamics #MMPMID27575707 Gibeault RL ; Conn KL ; Bildersheim MD ; Schang LM PLoS Pathog 2016[Aug]; 12 (8 ): e1005842 PMID27575707 show ga Although ICP4 is the only essential transcription activator of herpes simplex virus 1 (HSV-1), its mechanisms of action are still only partially understood. We and others propose a model in which HSV-1 genomes are chromatinized as a cellular defense to inhibit HSV-1 transcription. To counteract silencing, HSV-1 would have evolved proteins that prevent or destabilize chromatinization to activate transcription. These proteins should act as HSV-1 transcription activators. We have shown that HSV-1 genomes are organized in highly dynamic nucleosomes and that histone dynamics increase in cells infected with wild type HSV-1. We now show that whereas HSV-1 mutants encoding no functional ICP0 or VP16 partially enhanced histone dynamics, mutants encoding no functional ICP4 did so only minimally. Transient expression of ICP4 was sufficient to enhance histone dynamics in the absence of other HSV-1 proteins or HSV-1 DNA. The dynamics of H3.1 were increased in cells expressing ICP4 to a greater extent than those of H3.3. The dynamics of H2B were increased in cells expressing ICP4, whereas those of canonical H2A were not. ICP4 preferentially targets silencing H3.1 and may also target the silencing H2A variants. In infected cells, histone dynamics were increased in the viral replication compartments, where ICP4 localizes. These results suggest a mechanism whereby ICP4 activates transcription by disrupting, or preventing the formation of, stable silencing nucleosomes on HSV-1 genomes. |Animals [MESH] |Cell Line [MESH] |Chlorocebus aethiops [MESH] |Chromatin/*metabolism [MESH] |Fluorescent Antibody Technique [MESH] |Gene Expression Regulation, Viral/*genetics [MESH] |Herpes Simplex/*virology [MESH] |Herpesvirus 1, Human/genetics/metabolism/pathogenicity [MESH] |Histones/metabolism [MESH] |Humans [MESH] |Immediate-Early Proteins/*metabolism [MESH] |Transcription, Genetic [MESH] |Transfection [MESH] |Vero Cells [MESH]An Essential Viral Transcription Activator Modulates Chromatin Dynamic(epmc).pdf DeepDyve Pubget Overpricing