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10.1128/JVI.77.20.11186-11192.2003 http://scihub22266oqcxt.onion/10.1128/JVI.77.20.11186-11192.2003 C224960!224960!14512566     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Virol 2003 ; 77 (20): 11186-92 Nephropedia Template TP {{tp|p=14512566|t=2003. Borna Disease Virus Nucleoprotein Interacts with the Cdc2-Cyclin B1 Complex |pdf=|usr=}}{{14512566}} gab.com Text Borna Disease Virus Nucleoprotein Interacts with the Cdc2-Cyclin B1 Complex JO: J Virol http://www.kidney.de/pget.php?&tw=1&pmid=14512566 #FOAvip Transition from G2 to M phase, a cell cycle checkpoint, is regulated by the Cdc2-cyclin B1 complex. Here, we report that persistent infection with Borna disease virus (BDV), a noncytolytic RNA virus infecting the central nervous system, results in decelerated proliferation of infected host cells due to a delayed G2-to-M transition. Persistent BDV-infected rat fibroblast cells showed reduced proliferation compared to uninfected cells. In pull-down assays we observed an interaction of the viral nucleoprotein with the Cdc2-cyclin B1 complex. Transfection of the viral nucleoprotein but not of the phosphoprotein also results in decelerated proliferation. This phenomenon was found in BDV-susceptible primary rat fibroblast cells and also in primary mouse cells, which are not susceptible to BDV infection. This is the first evidence that the noncytolytic Borna disease virus can manipulate host cell functions via interaction of the viral nucleoprotein with mitotic entry regulators. BDV preferentially infects and persists in nondividing neurons. The present report could give an explanation for this selective choice of host cell by BDV. Twit Text FOAVip Borna Disease Virus Nucleoprotein Interacts with the Cdc2-Cyclin B1 Complex ????J Virol http://www.kidney.de/pget.php?&tw=1&pmid=14512566 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=14512566 #FOAvip English Wikipedia <ref>{{Cite pmid|14512566}}</ref> Borna Disease Virus Nucleoprotein Interacts with the Cdc2-Cyclin B1 Complex #MMPMID14512566 Planz O; Pleschka S; Oesterle K; Berberich-Siebelt F; Ehrhardt C; Stitz L; Ludwig S J Virol 2003[Oct]; 77 (20): 11186-92 PMID14512566show ga Transition from G2 to M phase, a cell cycle checkpoint, is regulated by the Cdc2-cyclin B1 complex. Here, we report that persistent infection with Borna disease virus (BDV), a noncytolytic RNA virus infecting the central nervous system, results in decelerated proliferation of infected host cells due to a delayed G2-to-M transition. Persistent BDV-infected rat fibroblast cells showed reduced proliferation compared to uninfected cells. In pull-down assays we observed an interaction of the viral nucleoprotein with the Cdc2-cyclin B1 complex. Transfection of the viral nucleoprotein but not of the phosphoprotein also results in decelerated proliferation. This phenomenon was found in BDV-susceptible primary rat fibroblast cells and also in primary mouse cells, which are not susceptible to BDV infection. This is the first evidence that the noncytolytic Borna disease virus can manipulate host cell functions via interaction of the viral nucleoprotein with mitotic entry regulators. BDV preferentially infects and persists in nondividing neurons. The present report could give an explanation for this selective choice of host cell by BDV. äBorna Disease Virus Nucleoprotein Interacts with the Cdc2-Cyclin B1 Co(epmc).pdf DeepDyve Pubget Overpricing