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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 signaling but was independent of the type I interferon receptor.
4 to block HAV infection in mice lacking a key interferon receptor.
5 nus-associated kinase 1 (JAK1) to the type I interferon receptor.
6 his DDR depends on signaling from the type I interferon receptor.
7 were similar in mice deficient in the type I interferon receptor.
8 ce thresholds in mice lacking the alpha/beta interferon receptor.
9 APAP metabolism in the absence of the type I interferon receptor.
10 gulatory factors (IRFs) or the common type I interferon receptor.
11 feron-beta, which signals through the type I interferon receptor.
12 iffers between receptor tyrosine kinases and interferon receptors.
13 hat K3 and K5 both specifically target gamma interferon receptor 1 (IFN-gammaR1) and induce its ubiqu
15 2Rbeta), IL-15 receptor alpha (IL-15Ralpha), interferon receptor 2, and prostaglandin E synthase.
16 ns, cloning of human IFN-alpha and IFN-beta, interferon receptors, activities and therapeutic uses of
18 e been implicated in signalling derived from interferon receptors, although their precise role in thi
20 signaling cascade is activated by the Type I interferon receptor and plays a critical role in interfe
21 nd FcgammaRs in macrophages inhibited type I interferon receptor and Toll-like receptor (TLR) signali
22 man colorectal cancer cells lacking specific interferon receptors and compared it to that of an NSP1
23 infected cells, Jak1 kinase associated with interferon receptors and Stat2 associated with the inter
25 -of-function mutations in the genes encoding interferon-receptor-associated Janus kinase 1 (JAK1) or
26 Tyk2-dependent signaling through the Type I interferon receptor but not Tyk2-independent signaling a
27 advantage of the species specificity of the interferon receptors by analyzing human IFN-alpha-induce
28 mice deficient in the A1 chain of the type I interferon receptor (CD118(-/-)) are susceptible to HSV-
29 We found that downregulation of the type I interferon receptor chain IFNAR1 occurs in human CRC and
30 2-4 is predicted to be another member of the interferon receptor-class II cytokine receptor family.
32 or 2.2 (IFNAR2.2) chains of the human type I interferon receptor complex to demonstrate that the inte
33 sms underlying down-regulation of the type I interferon receptor consisting of IFNAR1 and IFNAR2 subu
34 MAYV/IRES vaccination of immunocompetent and interferon receptor-defective mice resulted in protectio
36 nfection of AG129 mice (alpha/beta and gamma interferon receptor deficient) showed rapid spread and l
37 Engraftment with lymphocytes from type I interferon receptor-deficient (IFN-alphabetaR(-/-)) mice
39 r, the trpB mutant remains virulent in gamma interferon receptor-deficient (IFN-gammaR(-/-)) mice, de
40 infectious virions to susceptible type I/II interferon receptor-deficient (ifnagr-/-) C57BL/6 (AG6)
42 induced in C57Bl/6 wild-type (WT) and type 1 interferon receptor-deficient (KO) mice for 90 min follo
44 V71 (mEV71) capable of infecting 12-week-old interferon receptor-deficient AG129 mice and used the mo
45 sts in the liver of infected chimpanzees and interferon receptor-deficient Ifnar1(-/-) mice for many
46 57BL/6 mice and protects type I or type I/II interferon receptor-deficient mice against lethal ZIKV c
47 ot essential for RV7 vaccination since gamma interferon receptor-deficient mice were protected by RV7
48 1-day-old CD-1 mice, absence of virulence in interferon receptor-deficient mice, and lack of transmis
49 UNV, adult mice lacking alpha/beta and gamma interferon receptors developed disseminated infection an
50 kappaB; the presence or absence of the gamma interferon receptor did not exhibit discernible differen
51 After infection with D2S10, mice lacking interferon receptors died early without manifesting sign
52 nonuclear phagocytes or deficiency of type I interferon receptor diminishes PGE(2)-dependent T(reg) i
53 ination of IFNAR1, endocytosis of the type I interferon receptor, down-regulation of IFNAR1 levels, a
54 ectopically stimulating different intestinal interferon receptors during RV infection eliminates seve
55 , consistent with overexpression of the four interferon receptors encoded on chromosome 21, and propo
56 likely via increased gene dosage of the four interferon receptors encoded on chromosome 21, contribut
57 vitamin A modulates the expression of type I interferon receptor enhancing the antireplication effect
58 owed that while cells lacking the alpha/beta interferon receptor exhibited decreased levels of transc
59 that the IL-10R, unlike other members of the interferon receptor family, is highly effective in recru
62 he gamma interferon gene (Ifng) or the gamma interferon receptor gene (Ifngr) have been engineered.
66 acking the Ifnlr1 gene encoding the type III interferon receptor have demonstrated that signaling thr
67 e broad species specificity of orthopoxvirus interferon receptors, herpesvirus and poxvirus proteins
68 nal deletion of STING, or blockade of type I interferon receptor I restored the immunoinhibitory pote
69 ne the roles of cGAS, IRF3, IRF7, the type I interferon receptor (IFN-alpha and IFN-beta receptor sub
70 r to cytokine receptors (R), including gamma interferon receptor (IFN-gammaR), interleukin 1 receptor
71 litis of the great elastic arteries in gamma interferon receptor (IFN-gammaR)-deficient mice with a f
72 r1 was required for the expression of type 3 interferon receptor (Ifn-lambdar1) upon IAV infection by
73 form of the beta (betaL) subunits of type I interferon receptor (IFN-R) in mouse cells is sufficient
74 alpha/IFNAR1 and betaL/IFNAR2) of the type I interferon receptor (IFN-R) in the activation of signal
75 orted that mice lacking alpha/beta and gamma interferon receptors (IFN-alpha/betaR and -gammaR) unifo
76 ational analysis of the beta chain of type I interferon receptor (IFNalphaRbetaL/IFNAR2) revealed tha
77 europathogenesis of ZIKV infection in type I interferon receptor IFNAR knockout (Ifnar1 (-/-) ) mice,
80 ing the ability to signal through the type I interferon receptor (IFNAR(-/-)) cannot control the SPBN
81 , we identify the temporal window for type I interferon receptor (IFNAR) blockade to drive TSCM cell
82 duction of PD-1 in melanoma cells via type I interferon receptor (IFNAR) signaling and reversal of IC
84 meras were used to define the role of type I interferon receptor (IFNAR) signaling in regulating gILC
85 ces PDL-1 expression and does so in an alpha interferon receptor (IFNAR) signaling-dependent manner.
86 is initiated through activation of the alpha interferon receptor (IFNAR), regulates the expression of
87 ential stimulator of inflammation-the type I interferon receptor (IFNAR)-and its associated transcrip
91 describe tumor-induced degradation of type I interferon receptor IFNAR1 chain as a new immune-evasion
92 interferon alpha/beta, and mice lacking the interferon receptor (Ifnar1(-/-)) developed neurological
94 l receptors, Toll-like receptor 4 and type 1 interferon receptor (IFNAR1), that are required for IPC-
96 t intradermal infection of mice lacking both interferon receptors (Ifnar1(-/-);Ifngr1(-/-)) with as f
98 istically, knockdown of Hsa21-encoded type I interferon receptors, IFNARs, rescues the DS microglial
99 ed chronic disease in mice lacking the gamma interferon receptor (IFNgammaR(-/-)), v-cyclin.LacZ viru
100 nnate immunity genes, including the type III interferon receptor IFNLR1, through depletion of H3K36 d
101 We demonstrate that triplication of the interferon receptor (IFNR) gene cluster on chromosome 21
103 that B. burgdorferi infection induced type I interferon receptor (IFNR) signaling in lymph nodes in a
104 ation is most likely regulated by the Type I interferon receptor (IFNR)-associated Tyk-2 kinase, as s
105 ulation in mice with null mutations (-/-) in interferon receptors (IFNR) for type I IFNs (IFN-alpha/b
109 Priming of the host cell, through TLR4 and interferon receptors, induces caspase-11 expression, and
111 e results indicate that while the alpha/beta interferon receptor is needed to curb viral replication,
112 sh latency in the spleen, we infected type I interferon receptor knockout (IFN-alpha/betaR(-/-)) mice
113 ave previously shown that infection of gamma interferon receptor knockout (IFN-gamma R(-/-)) mice wit
116 of molnupiravir protected susceptible type I interferon receptor knockout (Ifnar1(-/-)) mice against
117 riptional response of wild-type (WT), type I interferon receptor knockout (IFNAR1-/-), and STAT1 knoc
118 he liver of these hepatocyte-specific type-I interferon receptor knockout mice (Ifnar1(DeltaHep)), re
119 disease development in alpha/beta and gamma interferon receptor knockout mice, including neurologica
120 by 6 hr of reperfusion in WT but not type 1 interferon receptor KO mice that were protected from IRI
122 on-alpha/beta receptor 1 chain of the type I interferon receptor, leading to attenuation of IFNalpha
123 ound that deficiency in signaling via type I interferon receptor led to deregulated activation of gro
125 is of TR339 in 129 Sv/Ev mice and alpha/beta interferon receptor null (IFN-alpha/betaR(-/-)) mice, we
126 n of the G50DblKo mutant by growth on type I interferon receptor null MEFs, infection of IFN-alpha/be
127 global alignment of TF confers homology with interferon receptors of the cytokine receptor super fami
130 orted that mice lacking alpha/beta and gamma interferon receptors permit high levels of DENV replicat
131 ungs of wild-type and immunodeficient (gamma interferon receptor-/-, Rag1-/-, and tumor necrosis fact
132 SFV-RDR infection of mice lacking alpha/beta interferon receptors resulted in widespread virus distri
133 cell-intrinsic Toll-like receptor and type 1 interferon receptor signaling, upregulated an IRF8-depen
134 ibition at 2 weeks correlated with increased interferon receptor signaling, which waned by 2 months o
136 ted with defects in the pathways involved in interferon-receptor signaling and in antigen presentatio
137 both ZAP70 and Lck to the nucleus following interferon receptor stimulation is demonstrated for the
139 1 (JAK1), tyrosine kinase 2 (Tyk2), and the interferon receptor subunit 1 (IFNAR1), resulting in cel
141 thal in the brains of adult mice lacking the interferon receptor, suggesting that the viruses can inf
142 embryonic fibroblasts lacking the alpha/beta interferon receptor, the gamma interferon receptor, or b
143 e receptor family (CRF2), which includes the interferon receptors, the interleukin (IL) 10 receptor,
144 pathway components, destabilizes the type I interferon receptor though ubiquitination, and consequen
146 Many of these signals operate downstream of interferon receptors to elicit inflammasome regulators,
149 , CD80, CD86, PD-L1, CD95 ligand, and type I interferon receptor), we report that IPE cells uniquely
152 on of MyD88 and signaling through the type I interferon receptor were critical for the ability of the
153 These observations suggest that JAKs provide interferon receptors with a critical catalytic signaling
154 amily of type I IFNs in that it binds to the interferon receptors with high affinity, conferring exce