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1 ecule in signal transduction from the type I interferon receptor.
2 r to couple another signaling pathway to the interferon receptor.
3 his DDR depends on signaling from the type I interferon receptor.
4 were similar in mice deficient in the type I interferon receptor.
5 ce thresholds in mice lacking the alpha/beta interferon receptor.
6 APAP metabolism in the absence of the type I interferon receptor.
7 gulatory factors (IRFs) or the common type I interferon receptor.
8 feron-beta, which signals through the type I interferon receptor.
9 iffers between receptor tyrosine kinases and interferon receptors.
10 hat K3 and K5 both specifically target gamma interferon receptor 1 (IFN-gammaR1) and induce its ubiqu
11 2Rbeta), IL-15 receptor alpha (IL-15Ralpha), interferon receptor 2, and prostaglandin E synthase.
12 ns, cloning of human IFN-alpha and IFN-beta, interferon receptors, activities and therapeutic uses of
14 e been implicated in signalling derived from interferon receptors, although their precise role in thi
16 signaling cascade is activated by the Type I interferon receptor and plays a critical role in interfe
17 nd FcgammaRs in macrophages inhibited type I interferon receptor and Toll-like receptor (TLR) signali
18 infected cells, Jak1 kinase associated with interferon receptors and Stat2 associated with the inter
20 -of-function mutations in the genes encoding interferon-receptor-associated Janus kinase 1 (JAK1) or
21 Tyk2-dependent signaling through the Type I interferon receptor but not Tyk2-independent signaling a
22 advantage of the species specificity of the interferon receptors by analyzing human IFN-alpha-induce
23 mice deficient in the A1 chain of the type I interferon receptor (CD118(-/-)) are susceptible to HSV-
24 We found that downregulation of the type I interferon receptor chain IFNAR1 occurs in human CRC and
25 2-4 is predicted to be another member of the interferon receptor-class II cytokine receptor family.
27 or 2.2 (IFNAR2.2) chains of the human type I interferon receptor complex to demonstrate that the inte
28 sms underlying down-regulation of the type I interferon receptor consisting of IFNAR1 and IFNAR2 subu
29 nfection of AG129 mice (alpha/beta and gamma interferon receptor deficient) showed rapid spread and l
30 Engraftment with lymphocytes from type I interferon receptor-deficient (IFN-alphabetaR(-/-)) mice
32 r, the trpB mutant remains virulent in gamma interferon receptor-deficient (IFN-gammaR(-/-)) mice, de
34 induced in C57Bl/6 wild-type (WT) and type 1 interferon receptor-deficient (KO) mice for 90 min follo
36 V71 (mEV71) capable of infecting 12-week-old interferon receptor-deficient AG129 mice and used the mo
37 57BL/6 mice and protects type I or type I/II interferon receptor-deficient mice against lethal ZIKV c
38 ot essential for RV7 vaccination since gamma interferon receptor-deficient mice were protected by RV7
39 UNV, adult mice lacking alpha/beta and gamma interferon receptors developed disseminated infection an
40 kappaB; the presence or absence of the gamma interferon receptor did not exhibit discernible differen
41 After infection with D2S10, mice lacking interferon receptors died early without manifesting sign
42 ination of IFNAR1, endocytosis of the type I interferon receptor, down-regulation of IFNAR1 levels, a
43 , consistent with overexpression of the four interferon receptors encoded on chromosome 21, and propo
44 likely via increased gene dosage of the four interferon receptors encoded on chromosome 21, contribut
45 vitamin A modulates the expression of type I interferon receptor enhancing the antireplication effect
46 owed that while cells lacking the alpha/beta interferon receptor exhibited decreased levels of transc
47 that the IL-10R, unlike other members of the interferon receptor family, is highly effective in recru
49 he gamma interferon gene (Ifng) or the gamma interferon receptor gene (Ifngr) have been engineered.
50 e broad species specificity of orthopoxvirus interferon receptors, herpesvirus and poxvirus proteins
51 r to cytokine receptors (R), including gamma interferon receptor (IFN-gammaR), interleukin 1 receptor
52 litis of the great elastic arteries in gamma interferon receptor (IFN-gammaR)-deficient mice with a f
53 form of the beta (betaL) subunits of type I interferon receptor (IFN-R) in mouse cells is sufficient
54 alpha/IFNAR1 and betaL/IFNAR2) of the type I interferon receptor (IFN-R) in the activation of signal
55 orted that mice lacking alpha/beta and gamma interferon receptors (IFN-alpha/betaR and -gammaR) unifo
56 ational analysis of the beta chain of type I interferon receptor (IFNalphaRbetaL/IFNAR2) revealed tha
57 europathogenesis of ZIKV infection in type I interferon receptor IFNAR knockout (Ifnar1 (-/-) ) mice,
59 ing the ability to signal through the type I interferon receptor (IFNAR(-/-)) cannot control the SPBN
60 ces PDL-1 expression and does so in an alpha interferon receptor (IFNAR) signaling-dependent manner.
61 is initiated through activation of the alpha interferon receptor (IFNAR), regulates the expression of
62 ential stimulator of inflammation-the type I interferon receptor (IFNAR)-and its associated transcrip
66 describe tumor-induced degradation of type I interferon receptor IFNAR1 chain as a new immune-evasion
67 interferon alpha/beta, and mice lacking the interferon receptor (Ifnar1(-/-)) developed neurological
69 l receptors, Toll-like receptor 4 and type 1 interferon receptor (IFNAR1), that are required for IPC-
71 ed chronic disease in mice lacking the gamma interferon receptor (IFNgammaR(-/-)), v-cyclin.LacZ viru
73 that B. burgdorferi infection induced type I interferon receptor (IFNR) signaling in lymph nodes in a
74 ation is most likely regulated by the Type I interferon receptor (IFNR)-associated Tyk-2 kinase, as s
75 ulation in mice with null mutations (-/-) in interferon receptors (IFNR) for type I IFNs (IFN-alpha/b
78 Priming of the host cell, through TLR4 and interferon receptors, induces caspase-11 expression, and
80 e results indicate that while the alpha/beta interferon receptor is needed to curb viral replication,
81 sh latency in the spleen, we infected type I interferon receptor knockout (IFN-alpha/betaR(-/-)) mice
82 ave previously shown that infection of gamma interferon receptor knockout (IFN-gamma R(-/-)) mice wit
85 riptional response of wild-type (WT), type I interferon receptor knockout (IFNAR1-/-), and STAT1 knoc
86 disease development in alpha/beta and gamma interferon receptor knockout mice, including neurologica
87 by 6 hr of reperfusion in WT but not type 1 interferon receptor KO mice that were protected from IRI
89 on-alpha/beta receptor 1 chain of the type I interferon receptor, leading to attenuation of IFNalpha
90 ound that deficiency in signaling via type I interferon receptor led to deregulated activation of gro
92 is of TR339 in 129 Sv/Ev mice and alpha/beta interferon receptor null (IFN-alpha/betaR(-/-)) mice, we
93 n of the G50DblKo mutant by growth on type I interferon receptor null MEFs, infection of IFN-alpha/be
94 global alignment of TF confers homology with interferon receptors of the cytokine receptor super fami
97 orted that mice lacking alpha/beta and gamma interferon receptors permit high levels of DENV replicat
98 ungs of wild-type and immunodeficient (gamma interferon receptor-/-, Rag1-/-, and tumor necrosis fact
99 SFV-RDR infection of mice lacking alpha/beta interferon receptors resulted in widespread virus distri
101 ted with defects in the pathways involved in interferon-receptor signaling and in antigen presentatio
102 both ZAP70 and Lck to the nucleus following interferon receptor stimulation is demonstrated for the
105 thal in the brains of adult mice lacking the interferon receptor, suggesting that the viruses can inf
106 embryonic fibroblasts lacking the alpha/beta interferon receptor, the gamma interferon receptor, or b
107 e receptor family (CRF2), which includes the interferon receptors, the interleukin (IL) 10 receptor,
109 Many of these signals operate downstream of interferon receptors to elicit inflammasome regulators,
112 , CD80, CD86, PD-L1, CD95 ligand, and type I interferon receptor), we report that IPE cells uniquely
115 These observations suggest that JAKs provide interferon receptors with a critical catalytic signaling
116 amily of type I IFNs in that it binds to the interferon receptors with high affinity, conferring exce
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