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1                                              NAIP CIIA HET-E and TP1 (NACHT) family proteins are invo
2                                              NAIP/NLRC4 inflammasome assembly is initiated by the bin
3                                              NAIPs (NLR family, apoptosis inhibitory proteins) are NL
4        However, how ligand binding activates NAIP is less clear.
5 f the human IAP family, c-IAP-1, c-IAP-2 and NAIP.
6 e activation in response to NLRP3, AIM2, and NAIP triggers when expressed in living cells, highlighti
7 d standard (n-nonadecane) for both NACME and NAIP esters were identical.
8 4/NOD1, NOD2/CARD15, CIAS1, CARD7/NALP1, and NAIP, in more detail.
9 y explaining the redundant role of NLRP3 and NAIP/NLRC4 during S. Typhimurium infection.
10 ed the possibility of alterations in SMN and NAIP in 154 patients with ALS (135 sporadic cases, 17 fa
11 calized the two SMA candidate genes, SMN and NAIP, to the Lgn1 critical region, making these two gene
12 ally have functional copies of both SMNT and NAIP.
13       Although metazoan paired NLRs, such as NAIP/NLRC4, form hetero-complexes upon activation, the m
14 ession of catalytically inactive JNK1 blocks NAIP and ML-IAP protection against ICE- and TNF-alpha-in
15 he intestinal epithelium when mice lack both NAIP-NLRC4 and Caspase-11.
16 le proteins (PrgI and homologs), detected by NAIP and the NLRC4 inflammasome.
17                              In THP-1 cells, NAIP/NLRC4 and NLRP3 played redundant roles in inflammas
18           We analyzed a panel of 43 chimeric NAIPs, allowing us to map the NAIP domain responsible fo
19 some sensing by not binding to their cognate NAIPs.
20                                 In contrast, NAIP failed to bind tightly to any of these proteases.
21  human macrophages remained unable to detect NAIP-evasive ligands even following priming.
22          Here we show in mice that different NAIP paralogues determine the specificity of the NLRC4 i
23 3SS structural proteins are thought to evade NAIP/NLRC4 inflammasome sensing by not binding to their
24 ted with SMA, it is not clear to what extent NAIP or other genes influence the SMA phenotype, or whet
25 rt that two other members of the IAP family, NAIP and ML-IAP, both activate JNK1.
26 ene products and CED-4) and NACHT (named for NAIP, CIIA, HET-E, and TEP1) subfamilies of the STAND NT
27 cal mechanism underlying the requirement for NAIP proteins by use of a reconstituted NLRC4 inflammaso
28  contrast, humans encode a single functional NAIP, raising the question of whether human NAIP senses
29 cription regulators) and NACHT NTPases (e.g. NAIP, TLP1, Het-E-1) that have been studied extensively
30 e neuronal apoptosis inhibitory protein gene NAIP, of the survival motor neuron gene SMN, and of a fu
31 the mantle convection process that generated NAIP magma with observations of the individual geologica
32    Patients with a low ratio also had higher NAIP and PYCARD messenger RNA levels after lipopolysacch
33 ultiple isoforms encoded by the single human NAIP gene.
34     Furthermore, we show that a single human NAIP isoform is capable of sensing the T3SS inner rod, n
35 erial ligands is conferred by a single human NAIP.
36                     Here, we show that human NAIP also senses the Salmonella Typhimurium T3SS inner r
37            Previous studies found that human NAIP detects both flagellin and the T3SS needle protein
38 ine NAIP1 is functionally analogous to human NAIP.
39  NAIP, raising the question of whether human NAIP senses one or multiple bacterial ligands.
40                         Our results identify NAIPs as immune sensor proteins and provide biochemical
41 duce pyroptosis in response to immunoevasive NAIP ligands, indicating that increased levels of NLRC4
42 pite strong biochemical evidence implicating NAIPs in specific detection of bacterial ligands, geneti
43 eal the mechanism of signal amplification in NAIP-NLRC4 inflammasomes.
44             Wildfire-associated increases in NAIP and the EPC0 persisted 6 and 7 years after wildfire
45 of apoptosis (IAP) family members, including NAIP, cIAP-1, cIAP-2, XIAP/hILP, survivin, and BRUCE, bl
46       The N-alkylated indanylidenepyrroline (NAIP) Schiff base 3 is an unnatural alpha-amino acid pre
47 d components of the canonical inflammasome - NAIP-NLRC4, NLRP3, NLRP1, CARD8 and caspase-1 - as well
48 e converted to NACME and N-acetyl-isopropyl (NAIP) esters; the latter established derivative was empl
49 ificantly different (KIE(NACME) = 1.036; KIE(NAIP) = 1.038) and were shown in both cases to be reprod
50         We generated knock-in mice that lack NAIP of MeCP2 and found that they performed better in hi
51 ession in murine macrophages, which licenses NAIP detection of evasive ligands.
52 thoxy N-methyl indanylidene-pyrrolinium (MeO-NAIP) in methanol.
53    However, when the solvent is removed, MeO-NAIP rotation is predicted to synchronize with a ring-in
54                         It is found that MeO-NAIP in methanol is incapable of exploiting the above me
55 R priming tunes the threshold for the murine NAIP/NLRC4 inflammasome to enable inflammasome responses
56 indings indicate that, in contrast to murine NAIPs, promiscuous recognition of multiple bacterial lig
57 n mouse and human is the Lgn1 candidate Naip/NAIP.
58 ined NOD-like receptors (NLRs): NODs, NALPs, NAIP and IPAF.
59 ctivate the best-studied NLRs (NLRP3, NLRC4, NAIP, and NLRP1) and in uncovering inflammasome NLRs.
60  including NLRP1, CARD8, NLRP3, NLRP6, NLRC4/NAIP, AIM2, pyrin, and caspases-4/-5/-11.
61 letion of NAIP, with a homozygous absence of NAIP exon 5.
62  the intestinal epithelium in the absence of NAIP-NLRC4.
63 ingle patient revealed a partial deletion of NAIP, with a homozygous absence of NAIP exon 5.
64 gand-bound state, the winged helix domain of NAIP forms a steric clash with NLRC4 to open it up.
65 of the mechanism and biological functions of NAIP/NLRC4 activation.
66                                  Knockout of NAIP or NLRC4 in THP-1 cells revealed that flagellin, bu
67 of spinal muscular atrophy while the loss of NAIP and perhaps other genes primarily affects the sever
68             These data indicate that loss of NAIP may affect disease severity and further, that the m
69  bystander apoptosis, while up-regulation of NAIP and cIAP2 mRNA suggest that EBOV has evolved additi
70 ight into species-specific TLR regulation of NAIP/NLRC4 inflammasome activation.
71 red for the subsequent co-oligomerization of NAIPs with the downstream signaling adaptor NLR family,
72 an macrophages are known to express only one NAIP gene, which detects the needle protein, but not rod
73 l either provide a novel function for SMN or NAIP or reveal the existence of another, yet uncharacter
74 higher levels of bioavailable particulate P (NAIP) - these effects were also observed downstream at l
75 tional roles of inflammasomes - particularly NAIP/NLRC4, NLRP6, and noncanonical caspase-4 (caspase-1
76 t neuronal activity-induced phosphorylation (NAIP) of methyl CpG-binding protein 2 (MeCP2) precedes i
77 of the National Agriculture Imagery Program (NAIP) and a LiDAR canopy height model; and (3) develop a
78 r the neuronal apoptosis inhibitory protein (NAIP) gene and a somewhat lesser fraction for the basal
79 f the neuronal apoptosis inhibitory protein (NAIP) gene are preferentially deleted in patients with s
80 gnition by NLR apoptosis inhibitory protein (NAIP) inflammasomes.
81 , the neuronal apoptosis inhibitory protein (NAIP).
82 SMN); Neuronal Apoptosis Inhibitory Protein (NAIP); and p44, a subunit of transcription factor II H (
83 ining family, apoptosis inhibitory proteins (NAIPs) activate the nucleotide-binding domain, leucine-r
84 he NLR family apoptosis inhibitory proteins (NAIPs) bind conserved bacterial ligands, such as the bac
85   NLR family, apoptosis inhibitory proteins (NAIPs) detect bacterial flagellin and structurally relat
86         The North Atlantic Igneous Province (NAIP) and Paleocene-Eocene Thermal Maximum (PETM) consti
87         The North Atlantic Igneous Province (NAIP) erupted in two major pulses that coincide with the
88         Mice express multiple highly related NAIP paralogs that recognize distinct bacterial proteins
89  is one of the rare carriers of SMA who show NAIP deletions, a further explanation is that the NAIP d
90 mbly is initiated by the binding of a single NAIP to its cognate ligand, but a subset of bacterial fl
91 some components such as NLRP3, AIM2, or some NAIPs, NLRC4 is constitutively present in resting macrop
92 at intestinal epithelial cell (IEC)-specific NAIP-NLRC4 activity is sufficient to protect mice from s
93 sults provide genetic evidence that specific NAIP proteins function to detect specific bacterial prot
94 mean STDV(NACME) = 0.3 per thousand and STDV(NAIP) = 0.4 per thousand).
95 me activation under conditions of suboptimal NAIP/NLRC4 activation, as observed in THP-1 cells, possi
96 esponses against immunoevasive or suboptimal NAIP ligands.
97 ochemical, and genetic data demonstrate that NAIP proteins are receptors for bacterial ligands, while
98                                 We find that NAIP-NLRC4-deficient mice are highly susceptible to oral
99                                We found that NAIP proteins control ligand-dependent oligomerization o
100                              We observe that NAIP-NLRC4 inflammasome activation in tuft cells leads t
101                     Our results suggest that NAIP of MeCP2 is required for modulating dynamic functio
102                                          The NAIP (NLR family apoptosis inhibitory protein)/NLRC4 (NL
103                                          The NAIP/NLRC4 inflammasome is a cytosolic sensor of bacteri
104                                          The NAIP/NLRC4 inflammasome is activated by multiple bacteri
105                                          The NAIP/NLRC4 inflammasomes activate caspase-1 in response
106 tivation of other inflammasomes, such as the NAIP (NLR family, apoptosis inhibitory protein)/NLRC4 in
107 ng that increased levels of NLRC4 enable the NAIP/NLRC4 inflammasome to detect these normally evasive
108 of 43 chimeric NAIPs, allowing us to map the NAIP domain responsible for specific ligand detection.
109 , a previously uncharacterized member of the NAIP gene family, whereas NAIP5 and NAIP6 activate NLRC4
110                            Activation of the NAIP-NLRC4 inflammasome initiates extrusion of infected
111 a is due to mouse-specific activation of the NAIP-NLRC4 inflammasome.
112  receptor-ligand model for activation of the NAIP-NLRC4 inflammasomes.
113 e North Atlantic during the formation of the NAIP.
114 pyroptosis by a mechanism independent of the NAIP/NLRC4 and caspase-1 axis.
115 hat genetic removal of one such pathway, the NAIP-NLRC4 inflammasome, is sufficient to convert mice f
116 flux of 0.2-0.5 PgC yr(-1) and show that the NAIP could have initiated PETM climate change.
117 deletions, a further explanation is that the NAIP deletion is in some way contributing to the ALS phe
118                       Here, we show that the NAIP, CIITA, HET-E, and TP1 (NACHT) domain of NLRP3 is t
119 ed greenhouse gas fluxes associated with the NAIP at sub-millennial resolution by linking measurement
120 KCdelta, ligand binding proteins such as the NAIPs, and caspase-11 and caspase-8 in addition to caspa
121 regions of the oligomerization domain of the NAIPs, rather than within the leucine-rich repeats, as w
122 the Google Earth Engine (GEE) platform using NAIP imagery and LiDAR-derived canopy height models.
123  death proteases, caspases-3 and -7, whereas NAIP presumably inhibits apoptosis via other targets.
124  with estimated Kis of <=0.1 microM, whereas NAIP did not.
125  a downstream adaptor that multimerizes with NAIPs to form an inflammasome.
126 poptosis (IAP) family (HIAP-1, HIAP-2, XIAP, NAIP, Survivin, and Livin).
127                           In addition, XIAP, NAIP, and JNK1 bind to TAK1.

 
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