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1 cient in Del-1 and LFA-1 or in Del-1 and the IL-17 receptor.
2 d tumor-associated stromal cells, which bear IL-17 receptors.
3                     G-CSF, its receptor, and IL-17 receptor A (IL-17RA) are all required to maintain
4 resent the crystal structure of a complex of IL-17 receptor A (IL-17RA) bound to IL-17F in a 1:2 stoi
5 didiasis underscore the preponderant role of IL-17 receptor A (IL-17RA) in preserving mucocutaneous i
6 ttenuates Crohn's disease, whereas IL-17A or IL-17 receptor A (IL-17RA) inhibition exacerbates Crohn'
7                  We have found that although IL-17 receptor A (IL-17RA)(-/-) mice were resistant to e
8       We demonstrate here that IL-23 and the IL-17 receptor A (IL-17RA), which mediates both IL-17A a
9 eneration of airway smooth muscle through an IL-17 receptor A (IL-17RA)-IL-17RC, nuclear factor kappa
10                                Inhibition of IL-17 receptor A did not produce a treatment effect in s
11 onses to IL-17A signaling, either because of IL-17 receptor A knockout or wild-type animals that rece
12 Apoe(-/-) mice by use of adenovirus-produced IL-17 receptor A reduced plaque burden in Apoe(-/-) mice
13 s by infecting C3H mice devoid of the common IL-17 receptor A subunit (IL-17RA) and thus deficient in
14 h brodalumab, a competitive inhibitor of the IL-17 Receptor A subunit.
15 n 11c (CD11c)/diphtheria toxin receptor, and IL-17 receptor A(-/-) mice were used to examine T-lympho
16 the fact that disruption of IL-17 signaling (IL-17 receptor A(-/-)) prevented airway neutrophilia in
17 ge peritoneal macrophages, were enriched for IL-17 receptor A, and for protumor and proangiogenic mol
18 ith BA, cholangiocytes were found to express IL-17 receptor A, and the prevalence of IL-17A(+) cells
19  gene expression in vitro, and this requires IL-17 receptor A, tumor necrosis factor receptor-associa
20 s evident in mice deficient in IL-17A or the IL-17 receptor A, which mediates IL-17A signaling, follo
21 t (Apoe(-/-)) mice with IL-17A-deficient and IL-17 receptor A-deficient mice to generate Il17a(-/-)Ap
22 interaction of IL-17A and/or IL-17F with the IL-17 receptor A/C (IL-17RA/C).
23                      Their interactions with IL-17 receptors A-E (IL-17RA-E) mediate host defenses wh
24                              Over-activating IL-17 receptors abnormally heightens responses to 21% ox
25  of IL-17 before challenge or absence of the IL-17 receptor abrogated the PA14DeltaaroA vaccine's pro
26 wed that in the absence of signaling via the IL-17 receptor adaptor protein Act-1, the protective eff
27 omain containing proteins, which include the IL-17 receptors and an adaptor protein Act1, have essent
28 ) T cells, signaling via the interleukin-17 (IL-17) receptor, and IL-22 production.
29       Because IL-17A and IL-17F, ligands for IL-17 receptor antagonist (IL-17RA), have been shown to
30 ged IFN-gamma(0) mice were treated with anti-IL-17 receptor antibody or sequentially with anti-IL-17
31 ly with anti-IL-17 antibody followed by anti-IL-17 receptor antibody.
32 subunit dynamics, and ligand contacts of the IL-17 receptor are poorly defined.
33 eta and IL-4 express high levels of mRNA for IL-17 receptor B (IL-17RB), the receptor for IL-25.
34      We found that mice deficient in IL-17A, IL-17 receptor C (IL-17RC), and adaptor protein Act1 (of
35 ts role in prostate cancers by interbreeding IL-17 receptor C (IL-17RC)-deficient mice with mice that
36                                              IL-17 receptor C and Pten double KO mice recapitulated t
37 ion of either IL-17 in RA synovial fluids or IL-17 receptor C on HMVECs significantly reduces the ind
38                                      Loss of IL-17 receptor C or Ab blockade of IL-17A was similarly
39 ube formation are mediated primarily through IL-17 receptor C.
40                 Act1 preferentially bound to IL-17 receptor complex, releasing its suppressive effect
41 tal in this setting and tested the impact of IL-17 receptor deficiency or antibody-mediated neutraliz
42                                              IL-17 receptor-deficient mice showed increased systemic
43                  On the other hand, Act1 and IL-17 receptor directly associate likely via homotypic i
44 stinct member of the IL-17 family that binds IL-17 receptor E/A to promote innate defense in epitheli
45        Furthermore, T cells deficient in the IL-17 receptor elicited an accelerated, aggressive wasti
46 rom septic human neonates, expression of the IL-17 receptor emerged as a critical regulatory node.
47 man fibroblasts and do not bind to the human IL-17 receptor extracellular domain.
48                                    The IL-17/IL-17 receptor family is the newest and least understood
49                     We demonstrate here that IL-17 receptor family shares sequence homology in their
50         IL-17C bound to IL-17RE, a member of IL-17 receptor family whose full-length isoform was sele
51 lar domain of members of the interleukin-17 (IL-17) receptor family.
52 talloproteinases, the signaling mechanism of IL-17 receptor has not been understood.
53 e formation of GCs and that mice lacking the IL-17 receptor have reduced GC B cell development and hu
54  protein termed EVI27/IL-17BR, which we term IL-17 receptor homolog 1 (IL-17Rh1) in light of the mult
55 ence and functional similarities, this novel IL-17 receptor homologue represents a potential human SE
56              Deficiency in IL-23, IL-17A, or IL-17 receptor (IL-17R) and mAb neutralization of CXCR2,
57                        Signaling through the IL-17 receptor (IL-17R) is required to prevent oropharyn
58                   Furthermore, the levels of IL-17 receptor (IL-17R) on the TRAF6-deficient EFs were
59 l involvement of the adaptor protein Act1 in IL-17 receptor (IL-17R) signaling and IL-17-dependent im
60                   Interleukin-17 (IL-17) and IL-17 receptor (IL-17R) signaling are essential for regu
61                         We hypothesized that IL-17 receptor (IL-17R) signaling is critical for G-CSF
62 s pathogen by disrupting IL-17 production or IL-17 receptor (IL-17R) signaling.
63 a U-box E3 ubiquitin ligase, is recruited to IL-17 receptor (IL-17R) upon IL-17 stimulation and is re
64 cted corneas from wild-type mice, those from IL-17 receptor (IL-17R)-deficient mice had significantly
65 ntibodies to VEGF were rendered sensitive in IL-17 receptor (IL-17R)-knockout hosts deficient in T(H)
66 estigated the role of interleukin-17 (IL-17)/IL-17 receptor (IL-17R)-mediated signaling in the protec
67 ported that female C57BL/6J mice lacking the IL-17 receptor (IL-17RA(KO)) are significantly more susc
68    The signaling mechanisms triggered by the IL-17 receptor (IL-17RA) and related receptors are strik
69 h interaction with its cognate receptor, the IL-17 receptor (IL-17RA).
70 we report that Act1, the key adaptor for the IL-17 receptor (IL-7R), formed a complex with the induci
71 okine receptor 2 (CXCR2) nor interleukin-17 (IL-17) receptor (IL-17R) deficiency changed the severity
72  was reversed in mice lacking both Del-1 and IL-17 receptor, indicating a crucial role for the IL-17/
73 L-17 is restricted to activated T cells, the IL-17 receptor is found to be widely expressed, a findin
74 ntly, we observed that the expression of the IL-17 receptor is significantly increased in CTCL skin l
75 w levels of corneal miR-132 were detected in IL-17 receptor knockout mice after HSV infection.
76 hen these cells were cultured with BMMs from IL-17 receptor knockout mice.
77 ar domain since deletion mutants missing the IL-17 receptor-like domain lack this inhibitory effect.
78 s, the function of other IL-17 cytokines and IL-17 receptor-like molecules is unclear.
79  Kras(G12D) induces expression of functional IL-17 receptors on PanIN epithelial cells and also stimu
80 ere, we confirmed that mice deficient in the IL-17 receptor or lacking the ability to secrete IL-17 a
81 17A or transplantation of grafts lacking the IL-17 receptor prevents disease.
82 ng the action of interleukin (IL) 17 with an IL-17 receptor (R):Fc fusion protein inhibits T-cell pro
83                     TPL2 acts by linking the IL-17 receptor signal to the activation of TAK1, which i
84 coded by Zc3h12a) is a feedback inhibitor of IL-17 receptor signal transduction.
85 r NEC development, as inhibition of STAT3 or IL-17 receptor signaling attenuated NEC in mice, while I
86                         Rather, mice lacking IL-17 receptor signaling had a cell-intrinsic impairment
87 se seemingly variegated processes by keeping IL-17 receptor signaling in check while supporting diffe
88        Cytokine-targeted strategies blocking IL-17 receptor signaling may be beneficial in asthma tre
89                             Mechanistically, IL-17 receptor signaling was required for the enhanced p
90 aB activator 1 (Act1), the key transducer of IL-17 receptor signaling, from the neuroectodermal linea
91                            In the absence of IL-17 receptor signaling, IL-17ra(-/-) mice had delayed
92                            In the absence of IL-17 receptor signaling, Il17ra(-/-) mice had significa
93 ion with segmented filamentous bacteria, and IL-17 receptor signaling.
94  or adaptive immunity (interleukin (IL)17-F, IL-17 receptor, STAT1, STAT3, antibodies to Th-17 cytoki
95                            To date, only one IL-17 receptor subunit has been identified, termed IL-17
96 pe IL-2Rbeta, including up-regulation of the IL-17 receptor subunit IL-17RA.
97 h ubiquitin ligase activity that couples the IL-17 receptor to downstream signaling pathways.
98 wn what molecule(s) directly associates with IL-17 receptor to initiate the signaling.
99 icate Act1 as a membrane-proximal adaptor of IL-17 receptor with an essential role in induction of in
100 ished the homotypic interaction of ACT1 with IL-17 receptors, with no effect on homodimerization.

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