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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 as substantially dependent on this TLR/IL-1R adaptor molecule.
6 transmits an activating signal via the DAP10 adaptor molecule.
7 tion and suggest the involvement of multiple adaptor molecules.
8 crotubule motors as well as actin-associated adaptor molecules.
9 ation, and the relative abundance of certain adaptor molecules.
10 ly required for the recruitment of signaling adaptor molecules.
11 function previously assigned exclusively to adaptor molecules.
12 substrate receptor proteins through specific adaptor molecules.
13 rocytic markers, and ionized calcium-binding adaptor molecule 1 (IBA1) as a constitutive microglial m
14 ry markers including ionized calcium-binding adaptor molecule 1 (Iba1), glial fibrillary acidic prote
15 w that the beta-arrestin1.signal-transducing adaptor molecule 1 (STAM1) complex, initially identified
18 ription factor 3 and ionized calcium binding adaptor molecule 1 for neurons and glia, respectively, a
19 -4(-/-), TLR-2/4(-/-), MyD88(-/-), MyD88/TLR adaptor molecule 1(-/-), interleukin-1 receptor [IL-1R1]
20 its adaptor protein TRIF (Toll-like receptor adaptor molecule 1) but does not require the MyD88 (myel
22 ta (4G8), microglia (ionized calcium binding adaptor molecule 1), astrocytes (glial fibrillary acidic
23 munostained with the ionized calcium-binding adaptor molecule 1; Iba-1) and the interaction of microg
24 ron (TRIF, also called TIR-domain-containing adaptor molecule-1 (TICAM-1)) is a signaling adaptor mol
25 adaptor protein Toll/IL-1R domain-containing adaptor molecule-1 (TRIF) did not develop larger brain d
26 tion and duration of ionized calcium-binding adaptor molecule-1-positive microglial reactivity in the
27 ntaining 2A (SH2D2A), and signal transducing adaptor molecule 2 (STAM2) as novel candidate adaptors t
28 that Rin1 interacts with signal-transducing adaptor molecule 2 (STAM2), a protein that associates wi
29 did not require TLRs 2, 4, or 9 or MyD88/TLR adaptor molecule 2 but did require MyD88, indicating a r
35 n which ICP0 promotes the degradation of TLR adaptor molecules and inhibition of the inflammatory res
36 it may perform this function by trafficking adaptor molecules and kinases to the pericentrosomal and
37 ifying the host sensors that detect WNV, the adaptor molecules and signaling pathways that regulate t
38 h the SH3 domain of STAM (signal transducing adaptor molecule)) and UBPY (ubiquitin isopeptidase Y) h
39 ntain the insulin receptor substrate (IRS) 1 adaptor molecule, and their formation requires the bindi
40 ng CD64 and FcepsilonR1alpha, with signaling adaptor molecules, and we confirm experimentally that eq
41 ium sensor protein hippocalcin, the clathrin adaptor molecule AP2, the postsynaptic density enriched
44 er PYHIN family members) associates with the adaptor molecule ASC (apoptosis-associated speck-like pr
45 ient in either caspase-1 or the inflammasome adaptor molecule ASC after rVSV immunization was not sig
47 by crossing with IL-1 receptor-deficient or adaptor molecule ASC-deficient mice, but not NLRP3-defic
49 und that ROMK bound directly to the clathrin adaptor molecule autosomal recessive hypercholesterolemi
50 ays of NF-kappaB activation and utilizes the adaptor molecule BCL10 (B-cell leukemia/lymphoma 10).
52 KG2C, NKp44, and NKp46, which associate with adaptor molecules bearing immunoreceptor tyrosine-based
55 erts its therapeutic effect by serving as an adaptor molecule between FKBP12 and the cell proliferati
57 actin cytoskeleton and because they serve as adaptor molecules between PSGL-1 and Syk, we examined th
58 ated substrate) and STAM (signal transducing adaptor molecule), both of which harbor multiple ubiquit
60 s indicate that PGC1alpha represents a novel adaptor molecule capable of recruiting the necessary tra
61 nd c-Kit are generally deemed as independent adaptor molecules capable of transducing cytokine-specif
63 ed mice, we found that signaling through the adaptor molecule caspase activation and recruitment doma
64 nction of IPS-1, an essential RIG-I and MDA5 adaptor molecule, completely disabled the innate antivir
65 t these limitations by the use of a chimeric adaptor molecule comprising the extracellular domains of
68 complexed with the IgG-specific CD64-IgE Fc adaptor molecule could provide a substitute for human re
69 cyte phosphoprotein of 76 kDa (SLP-76) is an adaptor molecule critical for immunoreceptor and integri
70 ic 'YEEP' motif that was able to recruit the adaptor molecule Crk-L and phosphatidylinositol-3-OH kin
71 d zebrafish genome to identify six different adaptor molecules: Dap10, Dap12, Cd3zeta, Cd3zeta-like,
72 with human TLRs and macrophages from TLR and adaptor molecule-deficient mice and evaluated macrophage
74 of full-length, unmutated Bcl10, a signaling adaptor molecule encoded by a gene found to translocate
75 ule (TRADD), the Fas-associated death domain adaptor molecule (FADD), caspase-8, TNFR-associated fact
76 e peptidoglycan recognition proteins and the adaptor molecules Fas-associated protein with a death do
77 cleotides that also serves a dual role as an adaptor molecule for a number of intracellular DNA recep
79 nitiated by liver-resident cells through the adaptor molecule for cytosolic RNA sensors, Mavs, and th
81 ary response gene 88 (MyD88) is an essential adaptor molecule for IL-1 as well as most Toll-like rece
82 esults indicate that TAX1BP1 functions as an adaptor molecule for Itch to target MAVS during RNA viru
83 lthough myeloid differentiation factor 88 an adaptor molecule for most TLRs, is important for protect
85 with SRY and hypothesized to function as an adaptor molecule for SRY by tethering the KAP1-NuRD-SETD
86 Fas-associated death domain (FADD) is an adaptor molecule for the death receptor subfamily of the
88 ivator 1alpha (PGC1alpha) serves as a unique adaptor molecule for the recruitment of additional coact
93 MyD88 is a common Toll-like receptor (TLR) adaptor molecule found to be essential for induction of
94 F2-induced ERK activation through binding to adaptor molecule GRB2 to interfere with its association
95 atory responses, and an involvement of other adaptor molecules has not been suggested in TLR5-depende
96 rn recognition receptors and their signaling adaptor molecules has recently emerged as an essential c
98 ds on NF-kappaB activation, partially on the adaptor molecule IFN-promoter stimulator-1 and the novel
99 o mycobacteria, the possible function of the adaptor molecule IL-1R-associated kinase (IRAK)-4 agains
101 ining a caspase-recruitment domain (ASC), an adaptor molecule important for TLR-mediated caspase-1 ac
106 ion have focused primarily on its role as an adaptor molecule in signaling pathways in the cytoplasm,
108 nt domain-containing protein 9 (CARD9) is an adaptor molecule in the cytosol of myeloid cells, requir
109 ntified full-length presenilin as a critical adaptor molecule in the dephosphorylation of VEGFR1.
112 ng recruiting domain (ASC)/PYCARD, a central adaptor molecule in the Nod-like receptor (NLR) pathway,
113 Here, we show that expression of MAVS, a key adaptor molecule in the RIG-I-like receptor RNA-sensing
114 inker for activation of T cells (Lat), a key adaptor molecule in the TCR signaling pathway, in T cell
116 s strongly suggest that Rip2 functions as an adaptor molecule in transducing signals from immune rece
117 ibution of pattern recognition receptors and adaptor molecules in immunity to malaria remains poorly
118 s (PI(3)Ks) are activated through associated adaptor molecules in response to G protein-coupled and t
119 does not associate with any known signaling adaptor molecule, including DAP10, DAP12, or the FcRgamm
120 omponents, these TLRs associate with several adaptor molecules, including myeloid differentiation fac
121 ith increased surface expression of critical adaptor molecules, including the growth factor receptor
122 e immune signaling pathway that includes the adaptor molecule interferon promoter stimulator 1 (IPS-1
123 As such, stimulator of IFN genes (STING), an adaptor molecule involved in cytosolic DNA sensing, is r
124 otein, CD2-associated protein (CD2AP), is an adaptor molecule involved in podocyte homeostasis that c
125 X-activation protein 12 (DAP12), a signaling adaptor molecule involved in signal transduction of acti
126 tance of the LPS receptor TLR4 and MyD88, an adaptor molecule involved in the activation of the major
132 nition responses, that controlling levels of adaptor molecules is a recurring strategy in regulating
133 shown to interact with a number of cytosolic adaptor molecules, it is possible that the interaction o
138 n-radixin-moesin (ERM) proteins, a family of adaptor molecules linking the cortical actin cytoskeleto
140 ells and that signaling through the helicase adaptor molecule MAVS (mitochondrial antiviral signaling
141 h recognize viral RNA and signal through the adaptor molecule MAVS (mitochondrial antiviral signaling
142 he present study, we found that MDA5 and its adaptor molecule MAVS are critical for type I interferon
144 ORF-9b targets the mitochondrial-associated adaptor molecule MAVS signalosome by usurping PCBP2 and
145 ensing pathway mediated by the mitochondrial adaptor molecule MAVS, the TLR3 adaptor TRIF, or the tra
146 re, we show that the mitochondria-associated adaptor molecule, MAVS, is required for optimal NLRP3 in
149 naling pathways by affecting the function of adaptor molecules may provide new strategies to countera
150 adaptor-inducing interferon-beta (TRIF), an adaptor molecule mediating TLR3 signaling and MyD88-inde
151 eceptors transduce their signals through the adaptor molecule MyD88 and members of the IL-1R-associat
154 vestigated the involvement of the common TLR adaptor molecule MyD88 in host responses to C. pneumonia
155 naling by Toll-like receptors and the common adaptor molecule MyD88 in intestinal epithelial homeosta
156 aling by toll-like receptor 4 and the common adaptor molecule MyD88 in the pathogenesis of atheroscle
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
170 vates two signaling pathways mediated by the adaptor molecules MyD88 and Toll/IL-IR domain-containing
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
176 s severely impaired in mice deficient in the adaptor molecule myeloid differentiation antigen 88 (MyD
177 Toll-like receptor 3 (TLR3), signal via the adaptor molecule myeloid differentiation factor 88 (MyD8
178 role of TLR2, TLR4, and TLR9 and the common adaptor molecule myeloid differentiation factor 88 (MyD8
179 l blood through a mechanism dependent on the adaptor molecule myeloid differentiation primary respons
180 ciated molecular patterns and signal through adaptor molecules, myeloid differentiation factor 88 (My
181 he purified, recombinant SH3.1 domain of the adaptor molecule noncatalytic region of tyrosine kinase
182 cking for protein kinases, phosphatases, and adaptor molecules obligate for resensitization and recyc
183 ffold for protein kinases, phosphatases, and adaptor molecules obligate for resensitization and recyc
188 containing adaptor-inducing IFN-beta-related adaptor molecule produced equivalent cytokines as wild-t
189 downstream signaling pathways and/or shared adaptor molecules, rather than through direct extracellu
190 rs NOD1 and NOD2 and their common downstream adaptor molecule, receptor interacting protein 2 (RIP2;
191 of the TLR-4 signaling adaptor TRIF-related adaptor molecule reduced nuclear factor-kappaB activity
194 al caspase recruitment domain (ASC) is a key adaptor molecule required for the inflammatory processes
196 daptor family that includes Rap1-interacting adaptor molecule (RIAM) and lamellipodin, proteins invol
197 ntially associated with Rap1-GTP-interacting adaptor molecule (RIAM) both in vitro and in vivo, which
198 e of Rap1-guanosine triphosphate-interacting adaptor molecule (RIAM) for talin-1 recruitment and thus
200 llipodin (MRL) protein (Rap1-GTP-interacting adaptor molecule (RIAM) or lamellipodin), talin and acti
201 l GTPases interact with Rap1-GTP-interacting adaptor molecule (RIAM), a member of the MRL (Mig-10/RIA
202 n of Rap1-guanosine triphosphate-interacting adaptor molecule (RIAM), a Rap1 effector, blocks this re
203 dent integrin regulator Rap1-GTP-interacting adaptor molecule (RIAM), the recruitment of talin into T
204 eractions--vinculin and Rap1-GTP-interacting adaptor molecule (RIAM)--in the formation and maturation
205 (Q204L) did not reverse Rap1-GTP-interacting adaptor molecule (RIAM)-dependent increases in cell adhe
208 ges by selective conditional deletion of the adaptor molecule Rictor inhibits the generation of M2 ma
214 ceptors have been shown to interact with the adaptor molecule SAP; however, subsequent intracellular
217 ion of the key T cell receptor (TCR)-coupled adaptor molecule SH2-domain-containing phosphoprotein of
219 elocytic leukemia zinc finger (PLZF) and the adaptor molecule signaling lymphocyte activation molecul
221 ative (XLP) disease due to deficiency in the adaptor molecule signaling lymphocytic activation molecu
222 hus, SARM appears to be unique among the TIR adaptor molecules, since it functions to restrict viral
225 our studies demonstrate a novel role for the adaptor molecule SLP-76 in regulating HIV-1 infection in
226 proximal signaling complex nucleated by the adaptor molecules SLP-76 and LAT1 is required for activa
228 We used timed deletion of the TCR-signaling adaptor molecule Src homology 2 domain-containing phosph
229 We demonstrate that signal transduction adaptor molecule STAM-1A interacts with C. elegans LOV-1
230 e with the SH3 domain of signal transduction adaptor molecule (STAM) (AMSH) is a conserved metallopro
232 Src homology 3 domain of signal transducing adaptor molecule (STAM)] was fused to the carboxyl termi
234 ates whether knocking down two important TLR adaptor molecules, such as myeloid differentiation prote
235 minal caspase recruitment domain (ASC) is an adaptor molecule that has recently been implicated in th
236 adaptor molecule-1 (TICAM-1)) is a signaling adaptor molecule that is critically involved in the Toll
237 s-induced signaling adaptor (VISA), a unique adaptor molecule that is essential for retinoic acid ind
238 receptor-associated factor (TRAF)2 is a key adaptor molecule that is known to mediate proinflammator
243 previously unknown requirement for MyD88, an adaptor molecule that mediates signals at most TLRs, for
244 -associated factor 6 (TRAF6) is an important adaptor molecule that mediates the TNFR family and inter
245 ptosis or "anoikis." TMS1/ASC is a bipartite adaptor molecule that participates in inflammatory and a
246 vation molecule-associated protein (SAP), an adaptor molecule that recruits Fyn to the signaling lymp
247 target cell through expression of ezrin, an adaptor molecule that tethers proteins to the actin cyto
248 aptor protein 12 (DAP12) is a trans-membrane adaptor molecule that transduces activating signals in N
249 alpha and TIR-containing motif 1 (SARM1), an adaptor molecule that we found to be directly involved i
250 g is negatively regulated by beta-arrestins, adaptor molecules that also activate different intracell
251 ic intracellular compartment is conducted by adaptor molecules that bind to target motifs within the
252 ociated factor (TRAF) 2 and TRAF6, which are adaptor molecules that couple TNF and interleukin-1 rece
254 tor substrate (IRS) proteins are cytoplasmic adaptor molecules that function as signaling intermediat
257 llection of regulatory RNA-binding proteins, adaptor molecules that link Brk to signaling pathways ge
258 A genes is essential for generating the tRNA adaptor molecules that link genetic sequence and protein
259 ells, as well as on the set of intracellular adaptor molecules that link NT signalling to distinct bi
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
270 Src and Syk families, which activate several adaptor molecules to trigger Ca(2+) release and, in turn
272 was determined using siRNA against the TLR3 adaptor molecule Toll/IL-1R homologous region-domain-con
273 proinflammatory pathway is dependent on the adaptor molecules Toll/IL-1 receptor domain-containing a
274 imilarly, macrophages from mice deficient in adaptor molecules Toll/IL-1R domain-containing adaptor-i
276 TNF-alpha, the TNFR-associated death domain adaptor molecule (TRADD), the Fas-associated death domai
278 R) family member, forms a complex containing adaptor molecules TRAF2 and TRAF3, ubiquitin-conjugating
279 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
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