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1 responds to increased phosphorylation of the viral core protein.
2 is B virus (HBV) life cycle, mediated by the viral core protein.
3 are immature intermediates that lack DNA and viral core proteins.
4 ation codon of pr65gag, the precursor of the viral core proteins.
5 into cells infected with VACV expressing the viral core protein A4 fused to yellow fluorescent protei
7 and characterized an interaction between the viral core protein and host protein within bgcn homolog
8 involve ubiquitination or methylation of the viral core protein and is not mediated by the nitric oxi
9 S-FLU) that can infect cells and express the viral core proteins and neuraminidase but cannot replica
10 bacterial wall, it has been postulated that viral core proteins assembled inside the viral head are
12 ent marker and a fluorescently tagged Vpr (a viral core protein) enables detection of single-virus fu
13 egion of micro1 continued to colocalize with viral core proteins in punctate structures, indicating t
16 viral core protein of Hepatitis C virus, the viral core protein of Classical Swine Fever virus, the t
17 e cleavage profiling previously, namely, the viral core protein of Hepatitis C virus, the viral core
18 lular and virus-induced mechanisms, with the viral core protein playing an important role in steatosi
21 w a temporal correlation between the loss of viral core protein VII from the adenovirus genome and a
22 hat the sensitization of cells to TNF by the viral core protein was not due to up-regulation of TNFR
24 iated with complete dephosphorylation of the viral core protein, which forms the nucleocapsid wherein
25 case of triacsin C, reduced stability of the viral core protein, which forms the virion nucleocapsid