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1 off-target binding to proteins such as PKR (RNA-activated protein kinase).
2 luding the expression of the double-stranded-RNA-activated protein kinase.
3 lpha subunit of eIF-2 by the double-stranded RNA-activated protein kinase.
4 tor-1 (IRF-1) but not IRF-2, double-stranded RNA-activated protein kinase, and inducible nitric-oxide
5 ndent protein kinase II, and double-stranded RNA-activated protein kinase as the enzymes responsible
6 or of the interferon-induced double-stranded RNA-activated protein kinase, as induced during ER stres
7 nly 200 ng (3 pmol) of human double-stranded RNA-activated protein kinase expressed in a mutant strai
8 enzymes, viperin, ISG20, and double-stranded-RNA-activated protein kinase, inhibited steps in viral p
9 a (eIF2alpha) kinase or PKR (double-stranded RNA-activated protein kinase)-like endoplasmic reticulum
10 g caused weak stimulation of double-stranded RNA-activated protein kinase-like endoplasmic reticulum-
11 ion of PERK-eIF2alpha (PERK: double-stranded RNA-activated protein kinase-like ER kinase; eIF2alpha:
12 ibroblasts deficient in the ER stress kinase RNA-activated protein kinase-like ER-resident kinase (PE
13 s replication in control and double-stranded RNA-activated protein kinase-null MEFs indicated that th
14 innate immune response, the double-stranded RNA activated protein kinase PKR phosphorylates the tran
15 f sequence homology with the double-stranded RNA-activated protein kinase PKR and its substrate, the
16 ined the involvement of double stranded (ds) RNA-activated protein kinase PKR in tunicamycin-induced
22 anslation inhibition through double-stranded RNA-activated protein kinase (PKR) and also through a ne
23 iting autophosphorylation of double-stranded RNA-activated protein kinase (PKR) and blocking phosphor
24 nterferon (IFN)-induced double-stranded (ds) RNA-activated protein kinase (PKR) and is an important r
25 both the interferon-induced, double-stranded-RNA-activated protein kinase (PKR) and the endoribonucle
27 of the interferon-inducible double-stranded RNA-activated protein kinase (PKR) has been reported in
28 ole of interferon-inducible, double-stranded RNA-activated protein kinase (PKR) in the induction of a
29 cognized nuclear function of double-stranded RNA-activated protein kinase (PKR) in the pathogenesis o
30 or of the interferon-induced double-stranded RNA-activated protein kinase (PKR) is a cellular protein
32 he interferon (IFN)-induced, double-stranded RNA-activated protein kinase (PKR) mediates the antivira
33 In contrast, induction of double-stranded RNA-activated protein kinase (PKR) mRNA and protein by I
35 ent or overexpression of the double-stranded RNA-activated protein kinase (PKR) significantly increas
36 he interferon (IFN)-induced, double-stranded RNA-activated protein kinase (PKR) via the PKR eukaryoti
37 lated, whereas expression of double-stranded RNA-activated protein kinase (PKR) was decreased by 55%
39 rt, we provide evidence that double-stranded RNA-activated protein kinase (PKR), a stress kinase, is
40 ein family that includes the double-stranded RNA-activated protein kinase (PKR), Drosophila Staufen a
41 latory factor 1 (IRF-1), the double-stranded RNA-activated protein kinase (PKR), or RNase L (RNase L)
42 ess responses, including the double-stranded RNA-activated protein kinase (PKR)-like endoplasmic reti
43 zyme 1alpha (IRE1alpha), and double-stranded RNA-activated protein kinase (PKR)-like ER kinase (PERK)
50 that the interferon-induced, double-stranded RNA-activated protein kinase, PKR, is responsible for re
54 in kinase 3 [MAPK3], MAP3K8, double-stranded RNA-activated protein kinase [PRKR], and MAP2K4), and of
56 nensis activates macrophage double-stranded, RNA-activated protein kinase R (PKR) to promote parasite
57 viral nonstructural proteins independent of RNA-activated protein kinase R and replication of HBoV1
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