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1 NAIP CIIA HET-E and TP1 (NACHT) family proteins are invo
2 NAIPs (NLR family, apoptosis inhibitory proteins) are NL
4 e activation in response to NLRP3, AIM2, and NAIP triggers when expressed in living cells, highlighti
7 ed the possibility of alterations in SMN and NAIP in 154 patients with ALS (135 sporadic cases, 17 fa
8 calized the two SMA candidate genes, SMN and NAIP, to the Lgn1 critical region, making these two gene
10 ession of catalytically inactive JNK1 blocks NAIP and ML-IAP protection against ICE- and TNF-alpha-in
15 ted with SMA, it is not clear to what extent NAIP or other genes influence the SMA phenotype, or whet
17 ene products and CED-4) and NACHT (named for NAIP, CIIA, HET-E, and TEP1) subfamilies of the STAND NT
18 cal mechanism underlying the requirement for NAIP proteins by use of a reconstituted NLRC4 inflammaso
19 contrast, humans encode a single functional NAIP, raising the question of whether human NAIP senses
20 cription regulators) and NACHT NTPases (e.g. NAIP, TLP1, Het-E-1) that have been studied extensively
21 e neuronal apoptosis inhibitory protein gene NAIP, of the survival motor neuron gene SMN, and of a fu
23 Furthermore, we show that a single human NAIP isoform is capable of sensing the T3SS inner rod, n
30 pite strong biochemical evidence implicating NAIPs in specific detection of bacterial ligands, geneti
33 of apoptosis (IAP) family members, including NAIP, cIAP-1, cIAP-2, XIAP/hILP, survivin, and BRUCE, bl
35 e converted to NACME and N-acetyl-isopropyl (NAIP) esters; the latter established derivative was empl
36 ificantly different (KIE(NACME) = 1.036; KIE(NAIP) = 1.038) and were shown in both cases to be reprod
38 indings indicate that, in contrast to murine NAIPs, promiscuous recognition of multiple bacterial lig
41 ctivate the best-studied NLRs (NLRP3, NLRC4, NAIP, and NLRP1) and in uncovering inflammasome NLRs.
44 of spinal muscular atrophy while the loss of NAIP and perhaps other genes primarily affects the sever
46 bystander apoptosis, while up-regulation of NAIP and cIAP2 mRNA suggest that EBOV has evolved additi
47 red for the subsequent co-oligomerization of NAIPs with the downstream signaling adaptor NLR family,
48 an macrophages are known to express only one NAIP gene, which detects the needle protein, but not rod
49 l either provide a novel function for SMN or NAIP or reveal the existence of another, yet uncharacter
50 higher levels of bioavailable particulate P (NAIP) - these effects were also observed downstream at l
51 tional roles of inflammasomes - particularly NAIP/NLRC4, NLRP6, and noncanonical caspase-4 (caspase-1
52 t neuronal activity-induced phosphorylation (NAIP) of methyl CpG-binding protein 2 (MeCP2) precedes i
53 r the neuronal apoptosis inhibitory protein (NAIP) gene and a somewhat lesser fraction for the basal
54 f the neuronal apoptosis inhibitory protein (NAIP) gene are preferentially deleted in patients with s
57 SMN); Neuronal Apoptosis Inhibitory Protein (NAIP); and p44, a subunit of transcription factor II H (
58 ining family, apoptosis inhibitory proteins (NAIPs) activate the nucleotide-binding domain, leucine-r
59 he NLR family apoptosis inhibitory proteins (NAIPs) bind conserved bacterial ligands, such as the bac
61 is one of the rare carriers of SMA who show NAIP deletions, a further explanation is that the NAIP d
62 sults provide genetic evidence that specific NAIP proteins function to detect specific bacterial prot
67 tivation of other inflammasomes, such as the NAIP (NLR family, apoptosis inhibitory protein)/NLRC4 in
68 of 43 chimeric NAIPs, allowing us to map the NAIP domain responsible for specific ligand detection.
69 , a previously uncharacterized member of the NAIP gene family, whereas NAIP5 and NAIP6 activate NLRC4
72 deletions, a further explanation is that the NAIP deletion is in some way contributing to the ALS phe
73 KCdelta, ligand binding proteins such as the NAIPs, and caspase-11 and caspase-8 in addition to caspa
74 regions of the oligomerization domain of the NAIPs, rather than within the leucine-rich repeats, as w
75 death proteases, caspases-3 and -7, whereas NAIP presumably inhibits apoptosis via other targets.
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