It is perplexing that the original data suggested a statistically significant positive association with risk, whereas the replication data suggested an inverse relationship.
Altogether, assuming that Huh7-derived cells and tamarin hepatocytes provide similar cellular factors involved in GBV-B genome replication, our data suggest that these adaptive mutations may act to facilitate a later step in the virus life cycle, possibly involving packaging and/or particle assembly.
Although further functional analyses are needed to understand the impact that expression of this variant has on DNA replication, these data suggest it may interfere with the normal function of Ciz1.
Although no marker passed stringent Bonferroni multiple testing and further analysis (e.g., haplotype based analysis) and replication is needed, this preliminary data suggests that our candidate gene selection approach might be effective.
mtDNA mutations were previously thought to be associated with increased oxidative damage, however recent data suggests early mitochondrial replication errors propagate with time [ 26].
Together this data suggests that a change in replication timing is also associated with a concerted change in both gene expression and the epigenetic status of the promoter.
Our data suggests that Tim functions at replication termination structures, as well as in subsequent mitotic events in close association with mitotic kinases.
Our data suggests that in order to reduce virus replication in hepatic cells, miR122-detargeting alone is effective but not efficient enough to completely attenuate virus replication.
Our data suggests that GCN5 has a major role in DNA replication.
Together our data suggests that long-range domains of transcriptional alterations in cancer are also associated with concordant alterations in replication timing.
Thus, our data suggests that the accessory proteins, i.e. 3a and 7a, could play an important role during the replication cycle of the SARS-CoV.
