ライフサイエンスコーパス: NAIP

1 NAIP CIIA HET-E and TP1 (NACHT) family proteins are invo

2 NAIPs (NLR family, apoptosis inhibitory proteins) are NL

3 f the human IAP family, c-IAP-1, c-IAP-2 and NAIP.

4 e activation in response to NLRP3, AIM2, and NAIP triggers when expressed in living cells, highlighti

5 d standard (n-nonadecane) for both NACME and NAIP esters were identical.

6 4/NOD1, NOD2/CARD15, CIAS1, CARD7/NALP1, and NAIP, in more detail.

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

9 ally have functional copies of both SMNT and NAIP.

10 ession of catalytically inactive JNK1 blocks NAIP and ML-IAP protection against ICE- and TNF-alpha-in

11 le proteins (PrgI and homologs), detected by NAIP and the NLRC4 inflammasome.

12 We analyzed a panel of 43 chimeric NAIPs, allowing us to map the NAIP domain responsible fo

13 In contrast, NAIP failed to bind tightly to any of these proteases.

14 Here we show in mice that different NAIP paralogues determine the specificity of the NLRC4 i

15 ted with SMA, it is not clear to what extent NAIP or other genes influence the SMA phenotype, or whet

16 rt that two other members of the IAP family, NAIP and ML-IAP, both activate JNK1.

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

22 ultiple isoforms encoded by the single human NAIP gene.

23 Furthermore, we show that a single human NAIP isoform is capable of sensing the T3SS inner rod, n

24 erial ligands is conferred by a single human NAIP.

25 Here, we show that human NAIP also senses the Salmonella Typhimurium T3SS inner r

26 Previous studies found that human NAIP detects both flagellin and the T3SS needle protein

27 ine NAIP1 is functionally analogous to human NAIP.

28 NAIP, raising the question of whether human NAIP senses one or multiple bacterial ligands.

29 Our results identify NAIPs as immune sensor proteins and provide biochemical

30 pite strong biochemical evidence implicating NAIPs in specific detection of bacterial ligands, geneti

31 eal the mechanism of signal amplification in NAIP-NLRC4 inflammasomes.

32 Wildfire-associated increases in NAIP and the EPC0 persisted 6 and 7 years after wildfire

33 of apoptosis (IAP) family members, including NAIP, cIAP-1, cIAP-2, XIAP/hILP, survivin, and BRUCE, bl

34 The N-alkylated indanylidenepyrroline (NAIP) Schiff base 3 is an unnatural alpha-amino acid pre

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

37 We generated knock-in mice that lack NAIP of MeCP2 and found that they performed better in hi

38 indings indicate that, in contrast to murine NAIPs, promiscuous recognition of multiple bacterial lig

39 n mouse and human is the Lgn1 candidate Naip/NAIP.

40 ined NOD-like receptors (NLRs): NODs, NALPs, NAIP and IPAF.

41 ctivate the best-studied NLRs (NLRP3, NLRC4, NAIP, and NLRP1) and in uncovering inflammasome NLRs.

42 letion of NAIP, with a homozygous absence of NAIP exon 5.

43 ingle patient revealed a partial deletion of NAIP, with a homozygous absence of NAIP exon 5.

44 of spinal muscular atrophy while the loss of NAIP and perhaps other genes primarily affects the sever

45 These data indicate that loss of NAIP may affect disease severity and further, that the m

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

55 gnition by NLR apoptosis inhibitory protein (NAIP) inflammasomes.

56 , the neuronal apoptosis inhibitory protein (NAIP).

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

60 Mice express multiple highly related NAIP paralogs that recognize distinct bacterial proteins

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

63 mean STDV(NACME) = 0.3 per thousand and STDV(NAIP) = 0.4 per thousand).

64 We found that NAIP proteins control ligand-dependent oligomerization o

65 Our results suggest that NAIP of MeCP2 is required for modulating dynamic functio

66 The NAIP/NLRC4 inflammasomes activate caspase-1 in response

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

70 receptor-ligand model for activation of the NAIP-NLRC4 inflammasomes.

71 pyroptosis by a mechanism independent of the NAIP/NLRC4 and caspase-1 axis.

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.

76 with estimated Kis of <=0.1 microM, whereas NAIP did not.

77 poptosis (IAP) family (HIAP-1, HIAP-2, XIAP, NAIP, Survivin, and Livin).

78 In addition, XIAP, NAIP, and JNK1 bind to TAK1.