Human Herpesvirus 6B Induces Cell Cycle Arrest Concomitant with p53 Phosphorylation and Accumulation in T Cells
AUTOR(ES)
Øster, Bodil
FONTE
American Society for Microbiology
RESUMO
We studied the interactions between human herpesvirus 6B (HHV-6B) and its host cell. Productive infections of T-cell lines led to G1/S- and G2/M-phase arrest in the cell cycle concomitant with an increased level and enhanced DNA-binding activity of p53. More than 70% of HHV-6B-infected cells did not bind annexin V, indicating that the majority of cells were not undergoing apoptosis. HHV-6B infection induced Ser20 and Ser15 phosphorylation on p53, and the latter was inhibited by caffeine, an ataxia telangiectasia mutated kinase inhibitor. Thus, a productive HHV-6B infection suppresses T-cell proliferation concomitant with the phosphorylation and accumulation of p53.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544083Documentos Relacionados
- E2F1 Induces Phosphorylation of p53 That Is Coincident with p53 Accumulation and Apoptosis
- Absence of p53 in Clara cells favours multinucleation and loss of cell cycle arrest
- Human Herpesvirus 6B Genome Sequence: Coding Content and Comparison with Human Herpesvirus 6A
- Phosphorylation of p53: a Novel Pathway for p53 Inactivation in Human T-Cell Lymphotropic Virus Type 1-Transformed Cells
- Human Parvovirus B19 Induces Cell Cycle Arrest at G2 Phase with Accumulation of Mitotic Cyclins