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1 on myeloid cells and associates with a novel adaptor molecule.
2 C maturation requires TLR2 and MyD88, a TLR2 adaptor molecule.
3 ptive immunity without the need for this TLR adaptor molecule.
4 yrosine kinases: Btk, Lyn, Syk, and the Blnk adaptor molecule.
5 tion and suggest the involvement of multiple adaptor molecules.
6 crotubule motors as well as actin-associated adaptor molecules.
7 ation, and the relative abundance of certain adaptor molecules.
8 ly required for the recruitment of signaling adaptor molecules.
9 function previously assigned exclusively to adaptor molecules.
10 rocytic markers, and ionized calcium-binding adaptor molecule 1 (IBA1) as a constitutive microglial m
11 is factor alpha, and ionized calcium binding adaptor molecule 1 (Iba1) expression levels in at least
12 ry markers including ionized calcium-binding adaptor molecule 1 (Iba1), glial fibrillary acidic prote
13 d within accumulated ionized calcium binding adaptor molecule 1 (Iba1)-positive microglia and Ly6C(+)
14 w that the beta-arrestin1.signal-transducing adaptor molecule 1 (STAM1) complex, initially identified
17 ription factor 3 and ionized calcium binding adaptor molecule 1 for neurons and glia, respectively, a
19 f CD68(+), F4/80(+), ionized calcium binding adaptor molecule 1(-) macrophages containing Congo red-s
20 -4(-/-), TLR-2/4(-/-), MyD88(-/-), MyD88/TLR adaptor molecule 1(-/-), interleukin-1 receptor [IL-1R1]
21 c protein (GFAP) and ionized calcium binding adaptor molecule 1(IBA1) immunostaining indicated morpho
22 he adaptor protein STAM1 (signal-transducing adaptor molecule 1) because disruption of the interactio
23 its adaptor protein TRIF (Toll-like receptor adaptor molecule 1) but does not require the MyD88 (myel
25 ta (4G8), microglia (ionized calcium binding adaptor molecule 1), astrocytes (glial fibrillary acidic
26 nificantly increased ionized calcium-binding adaptor molecule 1-positive microglial activation surrou
27 munostained with the ionized calcium-binding adaptor molecule 1; Iba-1) and the interaction of microg
28 ron (TRIF, also called TIR-domain-containing adaptor molecule-1 (TICAM-1)) is a signaling adaptor mol
29 adaptor protein Toll/IL-1R domain-containing adaptor molecule-1 (TRIF) did not develop larger brain d
30 crophage activation (Ionized calcium binding adaptor molecule-1 [Iba-1]) and interleukin-6 [IL-6]) an
31 tion and duration of ionized calcium-binding adaptor molecule-1-positive microglial reactivity in the
32 ntaining 2A (SH2D2A), and signal transducing adaptor molecule 2 (STAM2) as novel candidate adaptors t
33 that Rin1 interacts with signal-transducing adaptor molecule 2 (STAM2), a protein that associates wi
34 did not require TLRs 2, 4, or 9 or MyD88/TLR adaptor molecule 2 but did require MyD88, indicating a r
40 n which ICP0 promotes the degradation of TLR adaptor molecules and inhibition of the inflammatory res
41 it may perform this function by trafficking adaptor molecules and kinases to the pericentrosomal and
42 ifying the host sensors that detect WNV, the adaptor molecules and signaling pathways that regulate t
43 ng CD64 and FcepsilonR1alpha, with signaling adaptor molecules, and we confirm experimentally that eq
44 ium sensor protein hippocalcin, the clathrin adaptor molecule AP2, the postsynaptic density enriched
47 er PYHIN family members) associates with the adaptor molecule ASC (apoptosis-associated speck-like pr
48 ient in either caspase-1 or the inflammasome adaptor molecule ASC after rVSV immunization was not sig
50 by crossing with IL-1 receptor-deficient or adaptor molecule ASC-deficient mice, but not NLRP3-defic
52 und that ROMK bound directly to the clathrin adaptor molecule autosomal recessive hypercholesterolemi
53 ays of NF-kappaB activation and utilizes the adaptor molecule BCL10 (B-cell leukemia/lymphoma 10).
57 erts its therapeutic effect by serving as an adaptor molecule between FKBP12 and the cell proliferati
60 actin cytoskeleton and because they serve as adaptor molecules between PSGL-1 and Syk, we examined th
61 endosomes, we identified signal-transducing adaptor molecule-binding protein (STAMBP) and ubiquitin-
62 ated substrate) and STAM (signal transducing adaptor molecule), both of which harbor multiple ubiquit
64 s indicate that PGC1alpha represents a novel adaptor molecule capable of recruiting the necessary tra
65 nd c-Kit are generally deemed as independent adaptor molecules capable of transducing cytokine-specif
66 ed mice, we found that signaling through the adaptor molecule caspase activation and recruitment doma
68 nction of IPS-1, an essential RIG-I and MDA5 adaptor molecule, completely disabled the innate antivir
69 t these limitations by the use of a chimeric adaptor molecule comprising the extracellular domains of
72 complexed with the IgG-specific CD64-IgE Fc adaptor molecule could provide a substitute for human re
73 cyte phosphoprotein of 76 kDa (SLP-76) is an adaptor molecule critical for immunoreceptor and integri
74 ic 'YEEP' motif that was able to recruit the adaptor molecule Crk-L and phosphatidylinositol-3-OH kin
75 d zebrafish genome to identify six different adaptor molecules: Dap10, Dap12, Cd3zeta, Cd3zeta-like,
76 atural killer (NK) receptor NKG2D and the NK adaptor molecule DAP12, which promoted cytotoxicity agai
77 with human TLRs and macrophages from TLR and adaptor molecule-deficient mice and evaluated macrophage
79 stimulating signaling pathways that coax the adaptor molecule ezrin (EZR) to tether rPhe508del-Na(+)/
80 ule (TRADD), the Fas-associated death domain adaptor molecule (FADD), caspase-8, TNFR-associated fact
81 e peptidoglycan recognition proteins and the adaptor molecules Fas-associated protein with a death do
82 cleotides that also serves a dual role as an adaptor molecule for a number of intracellular DNA recep
83 nitiated by liver-resident cells through the adaptor molecule for cytosolic RNA sensors, Mavs, and th
85 ary response gene 88 (MyD88) is an essential adaptor molecule for IL-1 as well as most Toll-like rece
86 esults indicate that TAX1BP1 functions as an adaptor molecule for Itch to target MAVS during RNA viru
88 with SRY and hypothesized to function as an adaptor molecule for SRY by tethering the KAP1-NuRD-SETD
89 Fas-associated death domain (FADD) is an adaptor molecule for the death receptor subfamily of the
91 ivator 1alpha (PGC1alpha) serves as a unique adaptor molecule for the recruitment of additional coact
96 F2-induced ERK activation through binding to adaptor molecule GRB2 to interfere with its association
97 atory responses, and an involvement of other adaptor molecules has not been suggested in TLR5-depende
98 rn recognition receptors and their signaling adaptor molecules has recently emerged as an essential c
100 ds on NF-kappaB activation, partially on the adaptor molecule IFN-promoter stimulator-1 and the novel
101 o mycobacteria, the possible function of the adaptor molecule IL-1R-associated kinase (IRAK)-4 agains
103 ining a caspase-recruitment domain (ASC), an adaptor molecule important for TLR-mediated caspase-1 ac
108 ion have focused primarily on its role as an adaptor molecule in signaling pathways in the cytoplasm,
110 nt domain-containing protein 9 (CARD9) is an adaptor molecule in the cytosol of myeloid cells, requir
111 ntified full-length presenilin as a critical adaptor molecule in the dephosphorylation of VEGFR1.
114 ng recruiting domain (ASC)/PYCARD, a central adaptor molecule in the Nod-like receptor (NLR) pathway,
115 Here, we show that expression of MAVS, a key adaptor molecule in the RIG-I-like receptor RNA-sensing
116 inker for activation of T cells (Lat), a key adaptor molecule in the TCR signaling pathway, in T cell
118 ibution of pattern recognition receptors and adaptor molecules in immunity to malaria remains poorly
119 s (PI(3)Ks) are activated through associated adaptor molecules in response to G protein-coupled and t
121 does not associate with any known signaling adaptor molecule, including DAP10, DAP12, or the FcRgamm
122 omponents, these TLRs associate with several adaptor molecules, including myeloid differentiation fac
123 ith increased surface expression of critical adaptor molecules, including the growth factor receptor
124 e immune signaling pathway that includes the adaptor molecule interferon promoter stimulator 1 (IPS-1
125 nducing interferon-beta (TRIF), TRIF-related adaptor molecule, interferon regulatory factor 3 (IRF-3)
126 As such, stimulator of IFN genes (STING), an adaptor molecule involved in cytosolic DNA sensing, is r
127 otein, CD2-associated protein (CD2AP), is an adaptor molecule involved in podocyte homeostasis that c
128 X-activation protein 12 (DAP12), a signaling adaptor molecule involved in signal transduction of acti
129 tance of the LPS receptor TLR4 and MyD88, an adaptor molecule involved in the activation of the major
135 nition responses, that controlling levels of adaptor molecules is a recurring strategy in regulating
136 shown to interact with a number of cytosolic adaptor molecules, it is possible that the interaction o
141 n-radixin-moesin (ERM) proteins, a family of adaptor molecules linking the cortical actin cytoskeleto
143 ells and that signaling through the helicase adaptor molecule MAVS (mitochondrial antiviral signaling
144 h recognize viral RNA and signal through the adaptor molecule MAVS (mitochondrial antiviral signaling
145 he present study, we found that MDA5 and its adaptor molecule MAVS are critical for type I interferon
147 ORF-9b targets the mitochondrial-associated adaptor molecule MAVS signalosome by usurping PCBP2 and
148 ensing pathway mediated by the mitochondrial adaptor molecule MAVS, the TLR3 adaptor TRIF, or the tra
149 re, we show that the mitochondria-associated adaptor molecule, MAVS, is required for optimal NLRP3 in
152 naling pathways by affecting the function of adaptor molecules may provide new strategies to countera
153 adaptor-inducing interferon-beta (TRIF), an adaptor molecule mediating TLR3 signaling and MyD88-inde
154 eceptors transduce their signals through the adaptor molecule MyD88 and members of the IL-1R-associat
156 naling by Toll-like receptors and the common adaptor molecule MyD88 in intestinal epithelial homeosta
158 scription factors XBP1 and CHOP nor the TLR4 adaptor molecule MyD88 is necessary for caspase-8 activa
160 engagement, colocalization of Opn-i and the adaptor molecule MyD88 was associated with induction of
169 vates two signaling pathways mediated by the adaptor molecules MyD88 and Toll/IL-IR domain-containing
170 Toll-like receptor signalling through the adaptor molecules MyD88 and TRIF in turn mediates effici
171 ng TLR-7, type I IFN receptor, and CCR2, the adaptor molecules MyD88, IL-1R-associated kinase (IRAK)-
172 Toll-like receptors (TLRs) associate with adaptor molecules (MyD88, Mal/TIRAP, TRAM, and TRIF) to
173 LRs, the IL-1R, and the IL-18R, use a common adaptor molecule, MyD88, for transducing activation sign
177 s severely impaired in mice deficient in the adaptor molecule myeloid differentiation antigen 88 (MyD
178 Toll-like receptor 3 (TLR3), signal via the adaptor molecule myeloid differentiation factor 88 (MyD8
179 role of TLR2, TLR4, and TLR9 and the common adaptor molecule myeloid differentiation factor 88 (MyD8
180 l blood through a mechanism dependent on the adaptor molecule myeloid differentiation primary respons
182 ciated molecular patterns and signal through adaptor molecules, myeloid differentiation factor 88 (My
183 he purified, recombinant SH3.1 domain of the adaptor molecule noncatalytic region of tyrosine kinase
184 cking for protein kinases, phosphatases, and adaptor molecules obligate for resensitization and recyc
185 ffold for protein kinases, phosphatases, and adaptor molecules obligate for resensitization and recyc
190 containing adaptor-inducing IFN-beta-related adaptor molecule produced equivalent cytokines as wild-t
192 downstream signaling pathways and/or shared adaptor molecules, rather than through direct extracellu
193 rs NOD1 and NOD2 and their common downstream adaptor molecule, receptor interacting protein 2 (RIP2;
194 of the TLR-4 signaling adaptor TRIF-related adaptor molecule reduced nuclear factor-kappaB activity
195 range of activation receptors with distinct adaptor molecules require additional stimulation for IFN
198 al caspase recruitment domain (ASC) is a key adaptor molecule required for the inflammatory processes
200 daptor family that includes Rap1-interacting adaptor molecule (RIAM) and lamellipodin, proteins invol
201 ntially associated with Rap1-GTP-interacting adaptor molecule (RIAM) both in vitro and in vivo, which
202 e of Rap1-guanosine triphosphate-interacting adaptor molecule (RIAM) for talin-1 recruitment and thus
204 llipodin (MRL) protein (Rap1-GTP-interacting adaptor molecule (RIAM) or lamellipodin), talin and acti
205 l GTPases interact with Rap1-GTP-interacting adaptor molecule (RIAM), a member of the MRL (Mig-10/RIA
206 n of Rap1-guanosine triphosphate-interacting adaptor molecule (RIAM), a Rap1 effector, blocks this re
207 dent integrin regulator Rap1-GTP-interacting adaptor molecule (RIAM), the recruitment of talin into T
208 eractions--vinculin and Rap1-GTP-interacting adaptor molecule (RIAM)--in the formation and maturation
209 (Q204L) did not reverse Rap1-GTP-interacting adaptor molecule (RIAM)-dependent increases in cell adhe
212 ges by selective conditional deletion of the adaptor molecule Rictor inhibits the generation of M2 ma
219 ion of the key T cell receptor (TCR)-coupled adaptor molecule SH2-domain-containing phosphoprotein of
220 elocytic leukemia zinc finger (PLZF) and the adaptor molecule signaling lymphocyte activation molecul
222 ative (XLP) disease due to deficiency in the adaptor molecule signaling lymphocytic activation molecu
223 hus, SARM appears to be unique among the TIR adaptor molecules, since it functions to restrict viral
226 our studies demonstrate a novel role for the adaptor molecule SLP-76 in regulating HIV-1 infection in
227 proximal signaling complex nucleated by the adaptor molecules SLP-76 and LAT1 is required for activa
229 We used timed deletion of the TCR-signaling adaptor molecule Src homology 2 domain-containing phosph
230 We demonstrate that signal transduction adaptor molecule STAM-1A interacts with C. elegans LOV-1
231 e with the SH3 domain of signal transduction adaptor molecule (STAM) (AMSH) is a conserved metallopro
233 Src homology 3 domain of signal transducing adaptor molecule (STAM)] was fused to the carboxyl termi
236 ates whether knocking down two important TLR adaptor molecules, such as myeloid differentiation prote
237 adaptor molecule-1 (TICAM-1)) is a signaling adaptor molecule that is critically involved in the Toll
238 s-induced signaling adaptor (VISA), a unique adaptor molecule that is essential for retinoic acid ind
239 receptor-associated factor (TRAF)2 is a key adaptor molecule that is known to mediate proinflammator
244 previously unknown requirement for MyD88, an adaptor molecule that mediates signals at most TLRs, for
245 -associated factor 6 (TRAF6) is an important adaptor molecule that mediates the TNFR family and inter
246 ptosis or "anoikis." TMS1/ASC is a bipartite adaptor molecule that participates in inflammatory and a
247 vation molecule-associated protein (SAP), an adaptor molecule that recruits Fyn to the signaling lymp
248 target cell through expression of ezrin, an adaptor molecule that tethers proteins to the actin cyto
249 aptor protein 12 (DAP12) is a trans-membrane adaptor molecule that transduces activating signals in N
250 alpha and TIR-containing motif 1 (SARM1), an adaptor molecule that we found to be directly involved i
251 g is negatively regulated by beta-arrestins, adaptor molecules that also activate different intracell
252 ic intracellular compartment is conducted by adaptor molecules that bind to target motifs within the
253 ociated factor (TRAF) 2 and TRAF6, which are adaptor molecules that couple TNF and interleukin-1 rece
255 tor substrate (IRS) proteins are cytoplasmic adaptor molecules that function as signaling intermediat
258 llection of regulatory RNA-binding proteins, adaptor molecules that link Brk to signaling pathways ge
259 A genes is essential for generating the tRNA adaptor molecules that link genetic sequence and protein
260 activation and proliferation dependent upon adaptor molecules that mediate formation of the immunolo
261 human TLR that associates directly with the adaptor molecule TIR domain-containing adaptor inducing
262 iation primary response 88- and TRIF-related adaptor molecule/TIR domain-containing adapter-inducing
263 4 TLR genes (TLR1, TLR2, TLR4, TLR6) and the adaptor molecule TIRAP between 205 African American wome
266 n 4 TLR genes (TLR1, TLR2, TLR4, TLR6) and 2 adaptor molecules (TIRAP, MyD88) were associated with C.
269 ochips that can be decorated with switchable adaptor molecules to select for target proteins of inter
271 was determined using siRNA against the TLR3 adaptor molecule Toll/IL-1R homologous region-domain-con
272 proinflammatory pathway is dependent on the adaptor molecules Toll/IL-1 receptor domain-containing a
273 imilarly, macrophages from mice deficient in adaptor molecules Toll/IL-1R domain-containing adaptor-i
275 TNF-alpha, the TNFR-associated death domain adaptor molecule (TRADD), the Fas-associated death domai
277 R) family member, forms a complex containing adaptor molecules TRAF2 and TRAF3, ubiquitin-conjugating
278 ese findings show an unexpected role for the adaptor molecule TRAF6 in Smad-mediated TGF-beta signali
281 ing interferon-beta (TRIF), and TRIF-related adaptor molecule (TRAM) to activate transcription factor
282 ntiation protein 88 (MyD88) and TRIF-related adaptor molecule (TRAM), could affect mRNA expression of
283 erentiation protein (MyD88) and TRIF-related adaptor molecule (TRAM), using small interfering RNA abo
284 that TF4 binds to TLR4 but not TRIF-related adaptor molecule (TRAM), whereas TF5 binds to TRAM stron
286 ducing interferon-beta (TRIF)-, TRIF-related adaptor molecule (TRAM)-, and STING-deficient mice.
288 This stimulation leads to recruitment of the adaptor molecule TRIF (Toll/IL-1 resistance (TIR) domain
289 absence of caspase-8 activity, required the adaptor molecule TRIF, and proceeded in a cell autonomou
290 NA helicases DDX1, DDX21, and DHX36, and the adaptor molecule TRIF, by isolation and sequencing of po
293 pter-inducing interferon-beta (TRIF)-related adaptor molecule), TRIF, and MyD88, whereas A52 binds to
294 iating TLR3- or TLR4-induced signaling as an adaptor molecule, TRIF can participate in proteolytic mo
295 association of TLR4 with MD-2 and downstream adaptor molecules, TRIF and MyD88, into lipid rafts lead
298 Here, we introduce the concept of His-tagged adaptor molecules, which eliminate the need for the targ
299 domain protein 2 (Fhl2) is an intracellular adaptor molecule with a high protein-protein interaction