ライフサイエンスコーパス: PON

1 PON activity was assessed by quantification of nitrophen

2 PON also destroys biologically active, multioxygenated p

3 PON is asymmetrically localized during mitosis and coloc

4 PON-1 phenotype distribution and enzyme activities were

5 PON-1 status in patients with type 2 DM may contribute t

6 PON-1 was not associated directly with periodontitis.

7 PON-2 also co-immunoprecipitated with ENaC when co-expre

8 PON-2 did not alter the response of ENaC to extracellula

9 PON-2 shares key structural elements with MEC-6, an endo

10 and R61C significantly increased (p < 0.01) PON activity 32.6% +/- 14.7%, 31.6% +/- 18.9%, and 27.4%

11 Paraoxonase 1 (PON 1) is a serum glycoprotein associated with the high-

12 rmine the effects of tannase, paraoxonase-1 (PON-1) and/or cysteine protease (CP) on the copigmentati

13 AT (activity and expression), paraoxonase-1 (PON-1) expression and down-regulated heme oxygenase-1 (H

14 Paraoxonase-1 (PON-1) is involved in the prevention of atherosclerosis,

15 esterol efflux (P = 0.002) and paroxonase-1 (PON-1) activity (P < 0.0001) were lower, and serum amylo

16 PPARgamma induces macrophage paraoxonase 2 (PON-2), an enzyme that degrades QS molecules produced by

17 Paraoxonase-2 (PON-2) is a membrane-bound lactonase with unique anti-ox

18 O(9)](3-)) reacts with PyAOP ([(H(8)C(4)N)(3)PON(4)C(5)H(3)][PF(6)]) to yield an activated TriMP, [P(

19 sporadic ALS, we have identified at least 7 PON gene mutations that are predicted to alter PON funct

20 However, they have a PON-like gene with approximately 70% identity with human

21 N gene mutations that are predicted to alter PON function.

22 rrelated with TAC (r = -0.40, P < 0.02), and PON activity was positively correlated with TAC (r = 0.4

23 ic of 3OC12-HSL that is base-insensitive and PON-resistant.

24 POC and PON contents averaged 21.7 microg C pellet(-1) and 2.7 m

25 h PAO1 inhibited expression of PPARgamma and PON-2.

26 ts with DM, poor oral hygiene, male sex, and PON-1 phenotype were found to be significant predictors

27 ly oxidized LDL can induce an increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a

28 Furthermore, a dramatic increase in the apoJ/PON ratio (over 100-fold) was observed in LDL receptor k

29 resulting in a 9.2-fold increase in the apoJ/PON ratio as compared to controls.

30 n increased apoJ/PON ratio, and (b) the apoJ/PON ratio may prove to be a better predictor of atherosc

31 In contrast, the apoJ/PON ratio was 3.0+/-0.4 in the patients compared to 0.72

32 The arg192 PON isoform appears to be a risk factor in coronary arte

33 Serum paraoxonase/arylesterase (PON) is an "A" esterase found in the HDL2 fraction of ma

34 ON-2 inhibitory effect was ENaC-specific, as PON-2 had no effect on functional expression of the rena

35 Unlike the bacterial PON, the mammalian ancestor also hydrolyzes, with low ef

36 eport a newly identified family of bacterial PONs, and the reconstruction of the ancestor of the thre

37 e to a newly identified family of bacterial, PON-like "quorum-quenching" lactonases.

38 c studies have observed associations between PON gene polymorphisms and risk of cardiovascular diseas

39 wn that PAO1 QS molecules are inactivated by PON-2.

40 Phy and PhyloP) and 4 ensemble scores (CADD, PON-P, KGGSeq and CONDEL).

41 ate a possible correlation between decreased PON-1 activity and the association between impaired gluc

42 On an atherogenic diet, PON activity decreased by 52%, and apoJ levels increased

43 57BL/6J mice (IL-6 -/-) did not alter either PON activity or apoJ levels.

44 Moreover, ectopically expressed PON responds to the apical-basal polarity of epithelial

45 located, is the most ubiquitously expressed PON, and has the highest lactonase activity of the PON f

46 ive LDL) resulted in reduced mRNA levels for PON (3.0-fold decrease) and increased mRNA levels for ap

47 en proposed that apoA-I may be necessary for PON's association with plasma HDL.

48 l-2-(9'-oxo-nonanoyl)-glycerophosphocholine (PON-GPC).

49 ed the specific activities of purified human PONs for 3OC12-HSL hydrolysis, including the common PON1

50 ited by extended EDTA treatment, implicating PONs as the major enzymes inactivating 3OC12-HSL.

51 No changes in PON activity were observed with apoA-I cysteine substitu

52 on a chow diet resulted in a 59% decrease in PON activity (P < 0.01) and a 3.6-fold increase in apoJ

53 morphism and large individual differences in PON protein levels that are stable over time.

54 BL/6J mice resulted in a marked reduction in PON activity and an increase in apoJ levels in plasma af

55 ors result in large individual variations in PON serum levels, a substrate-dependent activity polymor

56 Lipid-free apoA-I did not increase PON activity, while preformed nascent HDL increased PON

57 ivity, while preformed nascent HDL increased PON activity only 30%, suggesting that maximal PON activ

58 rance of PAO1 in macrophages by PPARgamma is PON-2 dependent.

59 hylene oxide)-b-poly(N-isopropylacrylamide) (PON) triblock terpolymer and a poly(N-isopropylacrylamid

60 igating host-pathogen interactions and lacks PONs.

61 higher serum triglycerides (P = 0.02), lower PON-1 activity (P = 0.002) and higher prevalence of meta

62 gher titers of anti-HDL antibodies and lower PON activity than controls.

63 nificantly higher serum triglycerides, lower PON-1 activity and a higher prevalence of metabolic synd

64 base labile, and it is degraded by mammalian PON lactonases.

65 ancestor of the three families of mammalian PONs.

66 overlapping specificities of some mammalian PONs versus the singular specificity of others.

67 The mammalian PONs may therefore relate to a newly identified family o

68 N activity only 30%, suggesting that maximal PON activity is lipid-dependent and requires coassembly

69 tive, and low-cost sensor for point-of-need (PON) applications.

70 t as a promising standard for point-of-need (PON) assays in the GM industry.

71 tes of sinking particulate organic nitrogen (PON) from the euphotic zone are 2 - 3 orders of magnitud

72 modulation of the pretectal olivary nucleus (PON), which controls the pupillary light reflex; the sup

73 on of a novel gene product, Partner of Numb (PON), based on its physical interaction with Numb.

74 We observed PON-2 expression in aquaporin 2-positive principal cells

75 Extracellular accumulation of PON activity in the presence of apoA-I(WT) was 0.095 +/-

76 s lipid-dependent and requires coassembly of PON and apoA-I on nascent HDL.

77 This is due to a stepwise gelation of PON terpolymers involving micellization at room temperat

78 The expanded number of PON genes will have important implications for future ex

79 (2)GPI was the only independent predictor of PON activity (r = -0.483, P = 0.003).

80 o short term but not long term regulation of PON and that IL-6 is not required for OXPL regulation of

81 Since the physiologic role of PON is to prevent low-density lipoprotein oxidation with

82 The appearance of PONs in metazoa is likely to relate to innate immunity r

83 onary origins and substrate specificities of PONs therefore remain poorly understood.

84 of this, we examined the effect of apoA-I on PON's enzymatic activity and its ability to associate wi

85 The data suggest that, for optimal PON activity, coassembly of the enzyme onto nascent HDL

86 Recently, two other PON-like genes, designated "PON2" and "PON3," have been

87 Paraoxonase (PON) is transported primarily on apolipoprotein A-I (apo

88 Paraoxonase (PON), a high-density lipoprotein-associated enzyme, is b

89 L; apolipoprotein J (apoJ), and paraoxonase (PON).

90 ce 3OC12-HSL can be degraded by paraoxonase (PON) family members, we hypothesized that PONs regulate

91 protein J (apoJ), and decreased paraoxonase (PON) mRNA levels.

92 t two antioxidant-like enzymes, paraoxonase (PON)-1 and PON3, are high density lipoprotein-associated

93 phism at codon 192 in the human paraoxonase (PON) 1 gene has been shown to be associated with increas

94 as significantly reduced plasma paraoxonase (PON-1) activity, impaired HDL vascular antiinflammatory

95 drolytically inactivated by the paraoxonase (PON) family of calcium-dependent esterases, consisting o

96 The paraoxonase (PON) gene family includes three members, PON1, PON2, and

97 Paraoxonases (PONs) are a family of lactonases with promiscuous enzyme

98 Paraoxonases (PONs) are a family of proteins that may play a significa

99 Serum paraoxonases (PONs) are detoxifying lactonases that were first identif

100 Plasma PON activity was also significantly decreased, and apoJ

101 et both demonstrated markedly reduced plasma PON activities and the IL-6 -/- mice developed fatty str

102 on, particulate organic carbon/nitrogen (POC/PON), and sinking rates of fecal pellets produced by a f

103 In the SLE population, PON activity was inversely correlated with IgG anti-HDL

104 lar (MgON), tangential (TON), and posterior (PON) octaval nuclei, and the eminentia granularis (EG).

105 rolysis of tannins ["tannase," "lactonase (R-PON-1)"] and proteins (papain).

106 In "tannase + R-PON-1 + papain" treated PJ, turbidity decreased after st

107 2)GPI antibodies are associated with reduced PON activity in patients with SLE and primary APS.

108 is the first report that identifies a second PON enzyme in mammalian serum and the first to describe

109 "Tannase+PON-1" and "tannase+PON-1 + CP" caused a significant inc

110 "Tannase+PON-1" and "tannase+PON-1 + CP" caused a significant increase (8.8-12.1 %) i

111 lower cost, we recommend the use of "tannase+PON-1."

112 el (ENaC) is expressed, we hypothesized that PON-2 would similarly regulate ENaC expression.

113 Animal model studies indicate that PON activity levels are likely to play a major role in d

114 We propose that PON is one component of a multimolecular machinery that

115 Together, our data suggest that PON-2 regulates ENaC activity by modulating its intracel

116 rypsin-mediated proteolysis, suggesting that PON-2 did not alter the regulation of ENaC by these fact

117 e (PON) family members, we hypothesized that PONs regulate P. aeruginosa virulence in vivo.

118 These findings suggest that PONs, particularly PON2, could be an important mechanism

119 The PON-2 inhibitory effect was ENaC-specific, as PON-2 had

120 f these normolipidemic patients (n = 5), the PON activity was low (48+/-6.6 versus 98+/-17 U/ml for c

121 s describe a genetic association between the PON genes and sporadic amyotrophic lateral sclerosis (AL

122 ignificant association was found between the PON polymorphisms and stenosis severity in either white

123 e association between AD and variants in the PON gene cluster in Caucasians and African Americans.

124 affected by common genetic variation in the PON gene cluster, on chromosome 7.

125 ification of additional polymorphisms in the PON-gene cluster may help to locate the functional polym

126 nd has the highest lactonase activity of the PON family members.

127 Although the physiological roles of the PON family of proteins, PON1, PON2, and PON3, remain unk

128 Paraoxonase 3 (PON3) is a member of the PON family, which includes PON1, PON2, and PON3.

129 ion, and 2 kb of 3'-flanking sequence of the PON gene.

130 idation of the physiologic substrates of the PON proteins is of particular importance to further adva

131 arison to the NON copolymer, gelation of the PON terpolymer was achieved at a much lower concentratio

132 terval = 1.24 to 13.18; P = 0.02), and their PON-1 activity was reduced compared to controls.

133 ntiguous SNP combinations spanning the three PON genes with significant global test scores (0.006< or

134 use studies have demonstrated that all three PONs are atheroprotective.

135 When PON-2 was co-expressed with ENaC in Xenopus oocytes, ENa