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10.1371/journal.ppat.1006266 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1006266 28264028!5354443!28264028     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 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Pathog 2017 ; 13 (3): e1006266 Nephropedia Template TP {{tp|p=28264028|t=2017. Parvovirus B19 NS1 protein induces cell cycle arrest at G2-phase by activating the ATR-CDC25C-CDK1 pathway |pdf=|usr=}}{{28264028}} gab.com Text Parvovirus B19 NS1 protein induces cell cycle arrest at G2-phase by activating the ATR-CDC25C-CDK1 pathway JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28264028 #FOAvip Human parvovirus B19 (B19V) infection of primary human erythroid progenitor cells (EPCs) arrests infected cells at both late S-phase and G2-phase, which contain 4N DNA. B19V infection induces a DNA damage response (DDR) that facilitates viral DNA replication but is dispensable for cell cycle arrest at G2-phase; however, a putative C-terminal transactivation domain (TAD2) within NS1 is responsible for G2-phase arrest. To fully understand the mechanism underlying B19V NS1-induced G2-phase arrest, we established two doxycycline-inducible B19V-permissive UT7/Epo-S1 cell lines that express NS1 or NS1mTAD2, and examined the function of the TAD2 domain during G2-phase arrest. The results confirm that the NS1 TAD2 domain plays a pivotal role in NS1-induced G2-phase arrest. Mechanistically, NS1 transactivated cellular gene expression through the TAD2 domain, which was itself responsible for ATR (ataxia-telangiectasia mutated and Rad3-related) activation. Activated ATR phosphorylated CDC25C at serine 216, which in turn inactivated the cyclin B/CDK1 complex without affecting nuclear import of the complex. Importantly, we found that the ATR-CHK1-CDC25C-CDK1 pathway was activated during B19V infection of EPCs, and that ATR activation played an important role in B19V infection-induced G2-phase arrest. Twit Text FOAVip Parvovirus B19 NS1 protein induces cell cycle arrest at G2-phase by activating the ATR-CDC25C-CDK1 pathway ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=28264028 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28264028 #FOAvip English Wikipedia <ref>{{Cite pmid|28264028}}</ref> Parvovirus B19 NS1 protein induces cell cycle arrest at G2-phase by activating the ATR-CDC25C-CDK1 pathway #MMPMID28264028 Xu P; Zhou Z; Xiong M; Zou W; Deng X; Ganaie SS; Kleiboeker S; Peng J; Liu K; Wang S; Ye SQ; Qiu J PLoS Pathog 2017[Mar]; 13 (3): e1006266 PMID28264028show ga Human parvovirus B19 (B19V) infection of primary human erythroid progenitor cells (EPCs) arrests infected cells at both late S-phase and G2-phase, which contain 4N DNA. B19V infection induces a DNA damage response (DDR) that facilitates viral DNA replication but is dispensable for cell cycle arrest at G2-phase; however, a putative C-terminal transactivation domain (TAD2) within NS1 is responsible for G2-phase arrest. To fully understand the mechanism underlying B19V NS1-induced G2-phase arrest, we established two doxycycline-inducible B19V-permissive UT7/Epo-S1 cell lines that express NS1 or NS1mTAD2, and examined the function of the TAD2 domain during G2-phase arrest. The results confirm that the NS1 TAD2 domain plays a pivotal role in NS1-induced G2-phase arrest. Mechanistically, NS1 transactivated cellular gene expression through the TAD2 domain, which was itself responsible for ATR (ataxia-telangiectasia mutated and Rad3-related) activation. Activated ATR phosphorylated CDC25C at serine 216, which in turn inactivated the cyclin B/CDK1 complex without affecting nuclear import of the complex. Importantly, we found that the ATR-CHK1-CDC25C-CDK1 pathway was activated during B19V infection of EPCs, and that ATR activation played an important role in B19V infection-induced G2-phase arrest. |Ataxia Telangiectasia Mutated Proteins/metabolism[MESH] |Blotting, Western[MESH] |CDC2 Protein Kinase[MESH] |Cell Line[MESH] |Cyclin-Dependent Kinases/metabolism[MESH] |Erythroid Precursor Cells/virology[MESH] |Flow Cytometry[MESH] |G2 Phase Cell Cycle Checkpoints/*physiology[MESH] |Humans[MESH] |Immunoprecipitation[MESH] |Oligonucleotide Array Sequence Analysis[MESH] |Parvoviridae Infections/*metabolism[MESH] |Parvovirus B19, Human[MESH] |Signal Transduction/*physiology[MESH] |Viral Nonstructural Proteins/*metabolism[MESH]Parvovirus B19 NS1 protein induces cell cycle arrest at G2-phase by ac(epmc).pdf DeepDyve Pubget Overpricing