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Cation of a plasmid containing the JCV origin of replication. Using an in vivo approach with permissive PHFG cells, it was shown that JCV TAg is required for DNA replication, and JCV T9 proteins contribute to replication efficiency [45]. Further, a truncated JCV tAg mutant, encoding amino acids 1?9, replicated with similar efficiency to wild type JCV at days 7 and 14 p.t., but significant inhibiti
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Cation of a plasmid containing the JCV origin of replication. Using an in vivo approach with permissive PHFG cells, it was shown that JCV TAg is required for DNA replication, and JCV T9 proteins contribute to replication efficiency [45]. Further, a truncated JCV tAg mutant, encoding amino acids 1?9, replicated with similar efficiency to wild type JCV at days 7 and 14 p.t., but significant inhibiti
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Fference 0.0; 95 confidence interval [CI]: -8.7, 8.6). The eradication rates at the subject level for the microbiologically evaluable (ME) population were 79.2 in the tigecycline treatment group and 76.8 in the comparator treatment group (difference 2.4; 95 CI: -9.6, 14.4) at the TOC assessment. Nausea, vomiting, and diarrhea rates were higher in the tigecycline group. Conclusions: Tigecycline
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Cation of a plasmid containing the JCV origin of replication. Using an in vivo approach with permissive PHFG cells, it was shown that JCV TAg is required for DNA replication, and JCV T9 proteins contribute to replication efficiency [45]. Further, a truncated JCV tAg mutant, encoding amino acids 1?9, replicated with similar efficiency to wild type JCV at days 7 and 14 p.t., but significant inhibiti
1
Cation of a plasmid containing the JCV origin of replication. Using an in vivo approach with permissive PHFG cells, it was shown that JCV TAg is required for DNA replication, and JCV T9 proteins contribute to replication efficiency [45]. Further, a truncated JCV tAg mutant, encoding amino acids 1?9, replicated with similar efficiency to wild type JCV at days 7 and 14 p.t., but significant inhibiti
1
Cation of a plasmid containing the JCV origin of replication. Using an in vivo approach with permissive PHFG cells, it was shown that JCV TAg is required for DNA replication, and JCV T9 proteins contribute to replication efficiency [45]. Further, a truncated JCV tAg mutant, encoding amino acids 1?9, replicated with similar efficiency to wild type JCV at days 7 and 14 p.t., but significant inhibiti
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S this effect by blocking dephosphorylation of serines 120 and 123 [63,64]. However, SV40 tAg appears to stimulate SV40 replication to a limited extent in vivo; SV40 tAg deletion mutants produce slightly lower numbers of virions per infected cell [43] and addition of tAg protein to cells infected with SV40 tAg-defective genomes stimulates DNA replication [20]. Recently, tAg was shown to have a sig
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