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10.1128/jvi.77.5.2915-2921.2003 http://scihub22266oqcxt.onion/10.1128/jvi.77.5.2915-2921.2003 12584315!149759!12584315     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Virol 2003 ; 77 (5): 2915-21 Nephropedia Template TP {{tp|p=12584315|t=2003. Human parvovirus B19 nonstructural protein (NS1) induces cell cycle arrest at G(1) phase |pdf=|usr=}}{{12584315}} gab.com Text Human parvovirus B19 nonstructural protein (NS1) induces cell cycle arrest at G(1) phase JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=12584315 #FOAvip Human parvovirus B19 infects predominantly erythroid precursor cells, leading to inhibition of erythropoiesis. This erythroid cell damage is mediated by the viral nonstructural protein 1 (NS1) through an apoptotic mechanism. We previously demonstrated that B19 virus infection induces G(2) arrest in erythroid UT7/Epo-S1 cells; however, the role of NS1 in regulating cell cycle arrest is unknown. In this report, by using paclitaxel, a mitotic inhibitor, we show that B19 virus infection induces not only G(2) arrest but also G(1) arrest. Interestingly, UV-irradiated B19 virus, which has inactivated the expression of NS1, still harbors the ability to induce G(2) arrest but not G(1) arrest. Furthermore, treatment with caffeine, a G(2) checkpoint inhibitor, abrogated the B19 virus-induced G(2) arrest despite expression of NS1. These results suggest that the B19 virus-induced G(2) arrest is not mediated by NS1 expression. We also found that NS1-transfected UT7/Epo-S1 and 293T cells induced cell cycle arrest at the G(1) phase. These results indicate that NS1 expression plays a critical role in G(1) arrest induced by B19 virus. Furthermore, NS1 expression significantly increased p21/WAF1 expression, a cyclin-dependent kinase inhibitor that induces G(1) arrest. Thus, G(1) arrest mediated by NS1 may be a prerequisite for the apoptotic damage of erythroid progenitor cells upon B19 virus infection. Twit Text FOAVip Human parvovirus B19 nonstructural protein (NS1) induces cell cycle arrest at G(1) phase ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=12584315 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=12584315 #FOAvip English Wikipedia <ref>{{Cite pmid|12584315}}</ref> Human parvovirus B19 nonstructural protein (NS1) induces cell cycle arrest at G(1) phase #MMPMID12584315 Morita E; Nakashima A; Asao H; Sato H; Sugamura K J Virol 2003[Mar]; 77 (5): 2915-21 PMID12584315show ga Human parvovirus B19 infects predominantly erythroid precursor cells, leading to inhibition of erythropoiesis. This erythroid cell damage is mediated by the viral nonstructural protein 1 (NS1) through an apoptotic mechanism. We previously demonstrated that B19 virus infection induces G(2) arrest in erythroid UT7/Epo-S1 cells; however, the role of NS1 in regulating cell cycle arrest is unknown. In this report, by using paclitaxel, a mitotic inhibitor, we show that B19 virus infection induces not only G(2) arrest but also G(1) arrest. Interestingly, UV-irradiated B19 virus, which has inactivated the expression of NS1, still harbors the ability to induce G(2) arrest but not G(1) arrest. Furthermore, treatment with caffeine, a G(2) checkpoint inhibitor, abrogated the B19 virus-induced G(2) arrest despite expression of NS1. These results suggest that the B19 virus-induced G(2) arrest is not mediated by NS1 expression. We also found that NS1-transfected UT7/Epo-S1 and 293T cells induced cell cycle arrest at the G(1) phase. These results indicate that NS1 expression plays a critical role in G(1) arrest induced by B19 virus. Furthermore, NS1 expression significantly increased p21/WAF1 expression, a cyclin-dependent kinase inhibitor that induces G(1) arrest. Thus, G(1) arrest mediated by NS1 may be a prerequisite for the apoptotic damage of erythroid progenitor cells upon B19 virus infection. |Cell Cycle/*drug effects/physiology[MESH] |Cell Line[MESH] |Cyclin-Dependent Kinase Inhibitor p21[MESH] |Cyclins/metabolism[MESH] |G1 Phase/*drug effects/physiology[MESH] |Humans[MESH] |Parvoviridae Infections/*virology[MESH] |Parvovirus B19, Human/*pathogenicity/radiation effects[MESH] |Up-Regulation[MESH]Human parvovirus B19 nonstructural protein (NS1) induces cell cycle ar(epmc).pdf DeepDyve Pubget Overpricing