De Bolle Leen, Hatse Sigrid, Verbeken Erik, De Clercq Erik, Naesens Lieve
Rega Institute for Medical Research, Katholieke Universiteit Leuven, Minderbroedersstraat 10, B-3000 Leuven, Belgium.
FEBS Lett. 2004 Feb 27;560(1-3):25-9. doi: 10.1016/S0014-5793(04)00035-3.
We here report that after infection with human herpesvirus 6A, human cord blood mononuclear cells accumulate in G(2)/M phase of the cell cycle. Experiments with foscarnet or ultraviolet (UV)-irradiated virus stocks pointed at an (immediate-)early, newly formed viral protein to be responsible for the arrest. At the molecular level, p53, cyclin B(1), cyclin A and tyrosine(15)-phosphorylated cdk1 accumulated after HHV-6A infection, indicating an arrest in G(2). However, no change was observed in the levels of downstream effectors of p53 in establishing a G(2) arrest, i.e. p21 and 14-3-3sigma. We thus conclude that the HHV-6A-induced G(2) arrest occurs independently of p53 accumulation.
我们在此报告,人类脐带血单个核细胞在感染人类疱疹病毒6A后,会在细胞周期的G(2)/M期积累。使用膦甲酸钠或紫外线(UV)照射的病毒储备进行的实验表明,一种(即刻)早期新形成的病毒蛋白是导致细胞停滞的原因。在分子水平上,感染HHV-6A后,p53、细胞周期蛋白B(1)、细胞周期蛋白A和酪氨酸(15)磷酸化的cdk1会积累,表明细胞停滞在G(2)期。然而,在建立G(2)期停滞过程中,p53的下游效应分子p21和14-3-3sigma的水平未观察到变化。因此,我们得出结论,HHV-6A诱导的G(2)期停滞独立于p53积累而发生。