4,552 publications from this institution
A Convenient Route to 3′‐Deoxy‐α‐ L ‐ and 3′‐Deoxy‐β‐ D ‐apionucleosides The cyclic thionocarbonate 3 , easily available in three steps from 3′‐ O ‐benzoyl‐2,3‐ O ‐isopropylidene‐ D ‐apio‐β‐ D ‐furanose ( 1 ), is deoxygenated with n ‐Bu 3 SnH to yield the 3′‐deoxy epimers 4 [methyl 3‐C‐(benzoyloxymethyl)‐3‐deoxy‐α‐ L ‐ threo ‐tetrofuranoside] and 6 [methyl 3‐ C ‐(benzoyloxymethyl)‐3‐deoxy‐β‐ D ‐ erythro ‐tetrofuranoside]. These are separated by chromatography and further converted to the 3′‐deoxy‐α‐ L ‐apionucleosides 11–13 , and the 3′‐deoxy‐β‐ D ‐apionucleosides 17–19 , respectively.
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 14‐3‐3σ. We thus conclude that the HHV‐6A‐induced G 2 arrest occurs independently of p53 accumulation.
