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1 uced apoptosis by modulating the activity of double-stranded RNA-dependent protein kinase.
2 ctor 1, 2',5'-oligoadenylate synthetase, and double-stranded-RNA-dependent protein kinase as well as
4 oic acid + interferon-alpha --> upward arrow double-stranded RNA-dependent protein kinase --> downwar
5 R4-induced IFN-beta mRNA was MyD88- and PKR (double-stranded RNA-dependent protein kinase)-independen
7 implicated in the anti-viral response, e.g., double-stranded RNA-dependent protein kinase, myxovirus
8 vator of IL-1beta and IL-18 - as well as the double-stranded-RNA-dependent protein kinase pathway and
9 ble to bind to and inhibit activation of the double-stranded RNA-dependent protein kinase PKR in cell
10 es expression and autophosphorylation of the double-stranded RNA-dependent protein kinase PKR leading
16 -23 p40 and IFN-gamma, and the activation of double-stranded RNA-dependent protein kinase (PKR) and e
18 formation of SGs through the increase of the double-stranded RNA-dependent protein kinase (PKR) and f
19 d (iii) double-stranded RNA, which activates double-stranded RNA-dependent protein kinase (PKR) by mi
22 n as a result of repressed expression of the double-stranded RNA-dependent protein kinase (PKR) in th
24 lls infected with herpes simplex virus 1 the double-stranded RNA-dependent protein kinase (PKR) is ac
26 ed to be activated upon virus infection, the double-stranded RNA-dependent protein kinase (PKR) is be
27 imic the in vivo situation and show that the double-stranded RNA-dependent protein kinase (PKR) is in
28 In this study, we provide evidence that the double-stranded RNA-dependent protein kinase (PKR) is no
29 human tumor cells in which the activation of double-stranded RNA-dependent protein kinase (PKR) is su
30 vers, we discovered that viperin, ISG20, and double-stranded RNA-dependent protein kinase (PKR) noncy
31 ivation of c-Jun N-terminal kinase (JNK) and double-stranded RNA-dependent protein kinase (PKR) to in
33 ter activity, it promotes the degradation of double-stranded RNA-dependent protein kinase (PKR), and
34 and promotes the proteasomal degradation of double-stranded RNA-dependent protein kinase (PKR), litt
35 ough inhibiting eIF-2alpha kinases including double-stranded RNA-dependent protein kinase (PKR), whic
36 report that Ad-mda7 induces andactivates the double-stranded RNA-dependent protein kinase (PKR), whic
42 ease mechanisms, here we identify a role for double-stranded RNA-dependent protein kinase (PKR, also
43 Hri1p, Hri2p, or the human eIF2alpha kinase, double-stranded-RNA-dependent protein kinase (PKR), impe
45 trol of virus replication indicated that the double-stranded RNA-dependent protein kinase, PKR, exert
48 RNA and IFN-stimulated gene products such as double-stranded RNA-dependent protein kinase R (PKR), 2'
49 ing antiviral functions of the IFN-inducible double-stranded RNA-dependent protein kinase R or PKR.
51 fectivity was not restored in the absence of double-stranded RNA-dependent protein kinase, RNase L, o
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