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1 loads were similar in mice deficient in the type I interferon receptor.
2 crease APAP metabolism in the absence of the type I interferon receptor.
3 eron regulatory factors (IRFs) or the common type I interferon receptor.
4 g interferon-beta, which signals through the type I interferon receptor.
5 ter molecule in signal transduction from the type I interferon receptor.
6 on of this DDR depends on signaling from the type I interferon receptor.
8 kinase signaling cascade is activated by the Type I interferon receptor and plays a critical role in
9 grins and FcgammaRs in macrophages inhibited type I interferon receptor and Toll-like receptor (TLR)
10 inhibit Tyk2-dependent signaling through the Type I interferon receptor but not Tyk2-independent sign
11 t that mice deficient in the A1 chain of the type I interferon receptor (CD118(-/-)) are susceptible
14 receptor 2.2 (IFNAR2.2) chains of the human type I interferon receptor complex to demonstrate that t
15 Mechanisms underlying down-regulation of the type I interferon receptor consisting of IFNAR1 and IFNA
17 s, primary astrocytes, or BMM generated from type I interferon receptor-deficient (IFNAR(-/-)) mice.
18 ubiquitination of IFNAR1, endocytosis of the type I interferon receptor, down-regulation of IFNAR1 le
19 t that vitamin A modulates the expression of type I interferon receptor enhancing the antireplication
20 nd long form of the beta (betaL) subunits of type I interferon receptor (IFN-R) in mouse cells is suf
21 units (alpha/IFNAR1 and betaL/IFNAR2) of the type I interferon receptor (IFN-R) in the activation of
22 Mutational analysis of the beta chain of type I interferon receptor (IFNalphaRbetaL/IFNAR2) revea
23 e the neuropathogenesis of ZIKV infection in type I interferon receptor IFNAR knockout (Ifnar1 (-/-)
25 ce lacking the ability to signal through the type I interferon receptor (IFNAR(-/-)) cannot control t
26 an essential stimulator of inflammation-the type I interferon receptor (IFNAR)-and its associated tr
28 e the susceptibility of mice deleted for the type I interferon receptor (IFNAR-KO) to both HeV and Ni
29 et al. describe tumor-induced degradation of type I interferon receptor IFNAR1 chain as a new immune-
30 trated that B. burgdorferi infection induced type I interferon receptor (IFNR) signaling in lymph nod
31 sphorylation is most likely regulated by the Type I interferon receptor (IFNR)-associated Tyk-2 kinas
32 NAR(fl/fl) C57BL/6 (H-2(b)) mice lacking the type I interferon receptor in a subset of myeloid cells.
33 establish latency in the spleen, we infected type I interferon receptor knockout (IFN-alpha/betaR(-/-
34 transcriptional response of wild-type (WT), type I interferon receptor knockout (IFNAR1-/-), and STA
35 nterferon-alpha/beta receptor 1 chain of the type I interferon receptor, leading to attenuation of IF
36 re we found that deficiency in signaling via type I interferon receptor led to deregulated activation
37 lication of the G50DblKo mutant by growth on type I interferon receptor null MEFs, infection of IFN-a
42 0, CD47, CD80, CD86, PD-L1, CD95 ligand, and type I interferon receptor), we report that IPE cells un
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