The Rubella Virus Putative Replicase Interacts with the Retinoblastoma Tumor Suppressor Protein

摘要: In utero fetal infection of rubella virus (RV), a positive-stranded RNA virus, frequently induces birth defects if contracted in the first trimester pregnancy. The underlying mechanism RV-induced is not known. Birth are also common certain DNA viral infections such as human cytomegalovirus (HCMV). During HCMV infection, one its proteins interacts with cell growth regulatory protein, retinoblastoma protein (Rb) and stimulates synthesis which associated chromosomal damage cellular mitotic arrest. These affects have been implicated induced teratogenesis. Since RV both cause teratogenesis, we postulated that during virus-encoded might interact Rb affect growth. present study, identified known Rb-binding motif, L×C×E (LPCAE) carboxy-terminal half putative replicase (NSP90) demonstrated C-terminal region specifically binds to GST-Rb vitro. Further, by coimmunoprecipitating NSP90 using specific antibodies respective proteins, confirmed vivo well. addition, replication was shown be less null-mutant (Rb−/−) mouse embryonic fibroblast cells than wild-type (Rb+/+) cells, suggesting possible physiological role for this interaction. Thus, facilitating replication, binding potentially alters property Rb, could initial steps