ライフサイエンスコーパス: XOR

1 XOR bound to BTN1A1 orthologs from mice, humans, or cows

2 XOR is a member of the molybdoenzyme family and is best

3 XOR is required for butyrophilin1a1 clustering in the me

4 XOR loss alters the proteome of milk fat globules.

5 XOR mediates apical membrane reorganization during milk

6 XOR mRNA levels started to increase at mid-pregnancy, tu

7 XOR or squared Euclidean distance, by contrast, shows a

8 XOR requires molybdopterin, iron-sulphur centres, and FA

9 XOR returned to a diffuse cytoplasmic localization short

10 XOR-/- mice are runted and do not live beyond 6 wk of ag

11 confirmed the presence of eNOS and abundant XOR on whole RBCs.

12 Additionally, XOR can generate superoxide via NADH oxidase activity an

13 vented their adipogenic transformation in an XOR-dependent mechanism.

14 An "XOR" gate built using label-free, dual-analyte electroch

15 Therefore, we determined whether BTN1A1 and XOR directly interact using protein binding assays, surf

16 ing specific inhibitors of NADPH oxidase and XOR, prevented MCP-1 secretion.

17 amma isoforms and PPARgamma SUMOylation, and XOR inhibitors increased levels of SUMO-PPARgamma in MNP

18 A simple product of 1-Tanimoto and XOR tends to equalize the opposing size effects of the t

19 re isolated from mouse milk of wild-type and XOR MGKO dams, and subjected to LC-MS/MS for analysis of

20 ate that F-actin automata implement OR, AND, XOR and AND-NOT gates via interacting patterns of excita

21 N-terminal and C-terminal regions or between XOR subunits.

22 Although normal at birth, XOR-/- mice fail to thrive after 10 to 14 days, and most

23 a three-level circuit that exhibits Boolean XOR (exclusive OR) function.

24 Bovine XOR bound with high affinity in a pH- and salt-sensitive

25 The potential significance of BTN1A1/XOR interactions in the mammary gland and other tissues

26 d oxypurinol attenuate dysfunction caused by XOR in these disease states.

27 so observed that HIF-1alpha was increased by XOR inhibitors in inflammatory MNP and in MNP cell lines

28 Nonetheless, the role played by XOR during inflammation is poorly understood.

29 a show that increased O(2)(.-) production by XOR selectively uncouples eNOS activity and abolishes th

30 ntraction coupling in a manner reversible by XOR inhibition with allopurinol.

31 Together these data demonstrate that chronic XOR inhibition restores cardiac structure and function a

32 and AND gates, followed by the more complex XOR gate.

33 execute four steps of a logical (cumulative XOR) operation on a string of binary bits.

34 We detected XOR mRNA in HK-2 cells and confirmed its activity by ide

35 gates are produced, including the difficult XOR and EQUALS functions.

36 nic carbon, and unsaturation is required for XOR inhibition.

37 as acidosis develops, a substantial role for XOR becomes evident.

38 While a role for XOR beyond purine metabolism was first suggested in isch

39 epithelium, suggesting additional roles for XOR in these tissues.

40 one implementing the exclusive-or function (XOR) and another implementing what we refer to as an in-

41 Gate AND is the most common gate and gate XOR is the rarest.

42 The xanthine oxidoreductase gene (XOR) encodes an important source of reactive oxygen spec

43 Strikingly, however, XOR+/- females, although of healthy appearance and norma

44 We previously reported that basal human XOR (hXOR) expression is restricted or repressed by E-bo

45 A model is proposed to account for human XOR regulation.

46 Analysis of human XOR promoter activity in hepatocytes and vascular endoth

47 anthine oxidoreductase (XOR) have implicated XOR in many inflammatory diseases.

48 n leads to a global conformational change in XOR that results in the exposure of the region surroundi

49 suffering from xanthinuria, a deficiency in XOR, are potential candidates for lactation problems.

50 Here we have generated mice deficient in XOR.

51 (50-1,000 Da) for differential expression in XOR wildtype vs. mice with inactivated XOR, arising from

52 al NOS, NOS3) leads to profound increases in XOR-mediated O(2)(.-) production, which in turn depresse

53 ical and whole-mount analyses showed that in XOR+/- females the mammary epithelium collapses, resulti

54 on in XOR wildtype vs. mice with inactivated XOR, arising from gene deletion or pharmacological inhib

55 Importantly, SHHF rats exhibited increased XOR mRNA expression and activity, and oxypurinol treatme

56 number of disease states in which increased XOR activity plays a role.

57 a and suggest that strategies for inhibiting XOR may be valuable in modulating lung inflammatory diso

58 athways, supporting the idea that inhibiting XOR-derived oxidative stress substantially improves the

59 Nitro-oleic acid inhibits XOR activity in a concentration-dependent manner with an

60 These findings provide new insight into XOR functions and demonstrate the power of untargeted me

61 ic circuits such as NOT, AND, OR, NAND, NOR, XOR, and XNOR gates are demonstrated for performing mech

62 energy levels directly yields AND, OR, NOT, XOR, and even full addition logic operations with either

63 t the expression and membrane association of XOR in the mammary gland are tightly regulated by secret

64 gest that the apical membrane association of XOR regulates the coupling of lipid droplets to the apic

65 Association of XOR with the lipid droplet results in membrane docking a

66 ions in vivo to stabilize the association of XOR with the MFGM by direct interactions through the PRY

67 Mice with targeted disruption of XOR were generated to assess these potential additional

68 Gene expression of XOR is regulated by oxygen tension, cytokines and glucoc

69 Chronic inhibition of XOR and a diet deficient in nitrate/nitrite each exacerb

70 ondary nitrating species, with inhibition of XOR proving beneficial in a variety of disorders.

71 Inhibition of XOR reduced levels of CINC-1 secreted by MNP.

72 We previously observed that inhibition of XOR within the inflammatory mononuclear phagocytes (MNP)

73 a novel role for OA-NO2 in the inhibition of XOR-derived oxidant formation.

74 f nitrite were counteracted by inhibition of XOR.

75 examined the expression and localization of XOR in the non-secretory states of late pregnancy and in

76 al membrane, suggesting that localization of XOR is not dependent on the presence of Btn in the apica

77 Loss of XOR delays milk fat globule secretion.

78 Proteomic results showed that loss of XOR leads to an increase in cytoplasmic, cytoskeletal, G

79 Loss of XOR then results in a reversion to a more rudimentary, l

80 Both ectopic overexpression of XOR cDNA and uric acid supplementation reduced SUMO-PPAR

81 Attention to the broader range of XOR bioactivity in the cardiovascular system has prompte

82 adoptive transfer demonstrating the role of XOR in MNP-mediated neutrophil recruitment.

83 To further explore the role of XOR in the inflammatory state of MNP, we studied MNP iso

84 Binding was stoichiometric, with one XOR dimer binding to either two BTN1A1 monomers or one d

85 milar reduction in myocardial O(2)(.-), only XOR inhibition reduced eNOS S-glutathionylation and Ser-

86 wo-input-one-output logic gates (e.g. AND or XOR) to describe triplets of two factors regulating a co

87 ies of logic operations composed of AND, OR, XOR, complement, shift and addition.

88 s that emulate various logic gates (AND, OR, XOR, NAND, NOT, CNOT and a half adder).

89 realized permanent amplifying AND, NAND, OR, XOR, NOR, and XNOR gates actuated across common control

90 rforms various Boolean logic operations (OR, XOR, AND-OR) upon addition of glucose and/or H2O2 and ap

91 e basis for the low xanthine oxidoreductase (XOR) activity in humans relative to nonprimate mammalian

92 in 1A1 (BTN1A1) and xanthine oxidoreductase (XOR) are highly expressed in the lactating mammary gland

93 s further implicate xanthine oxidoreductase (XOR) as a source of reactive oxygen species in the cardi

94 Xanthine oxidoreductase (XOR) generates proinflammatory oxidants and secondary ni

95 this mechanism, and xanthine oxidoreductase (XOR) has long been thought to be functionally important.

96 gical inhibitors of xanthine oxidoreductase (XOR) have implicated XOR in many inflammatory diseases.

97 be suppressed with xanthine oxidoreductase (XOR) inhibition (i.e., allopurinol) or nitric oxide dono

98 Allopurinol, a xanthine oxidoreductase (XOR) inhibitor, abrogated the protective effects of nitr

99 As xanthine oxidoreductase (XOR) is 1 of the major sources of ROS, we tested whether

100 Xanthine oxidoreductase (XOR) is a 300-kDa homodimer that can exist as an NAD+-de

101 tudies suggest that xanthine oxidoreductase (XOR) is an important nitrite reductase in the heart and

102 Xanthine oxidoreductase (XOR) is the enzyme responsible for the final step in pur

103 Xanthine oxidoreductase (XOR) is the rate-limiting enzyme in purine catabolism oc

104 Xanthine oxidoreductase (XOR) modulates milk lipid secretion and lactation initia

105 hough inhibitors of xanthine oxidoreductase (XOR) or NOX2 NADPH oxidase caused a similar reduction in

106 Xanthine oxidoreductase (XOR), a key enzyme of purine metabolism, has been implic

107 increased levels of xanthine oxidoreductase (XOR), a known nitrite reductase.

108 we demonstrate that xanthine oxidoreductase (XOR), a prototypic superoxide O(2)(.-) -producing enzyme

109 rom inactivation of xanthine oxidoreductase (XOR), an enzyme that catalyzes the final steps in purine

110 ol, an inhibitor of xanthine oxidoreductase (XOR), blocks the oxidation of xanthine to urate.

111 f uric acid through xanthine oxidoreductase (XOR).

112 proportionation, or xanthine oxidoreductase (XOR).

113 upstream activator xanthine-oxidoreductase (XOR).

114 -studied mammalian xanthine oxidoreductases (XOR) and aldehyde oxidoreductases (AOR) and suggests a u

115 In contrast, during this same period, XOR-/- animals fail to augment renal COX-2 expression.

116 d activity, and oxypurinol treatment reduced XOR activity and superoxide production toward normal, bu

117 t an approximately 30-fold increase in renal XOR activity, with a corresponding induction of COX-2 ex

118 Here we review XOR gene structure and regulation, protein structure, en

119 We generated mammary-specific XOR knockout (MGKO) mice, expecting lactation to fail.

120 These results demonstrate that XOR activity is an endogenous physiological regulator of

121 These data demonstrate that XOR promotes the inflammatory state of MNP through effec

122 We demonstrated that XOR activity was increased in inflammatory MNP following

123 We present evidence that XOR may have primarily a structural role, as a membrane-

124 lk fat globule membrane proteins showed that XOR formed a sulphydryl-bond-dependent complex with Btn

125 Electron microscopy showed that XOR is specifically required for enveloping milk fat dro

126 otective effects of nitrite, suggesting that XOR is a key enzyme in the conversion of nitrite to nitr

127 and but not in the knockout, suggesting that XOR mediates 'docking' to this membrane.

128 nthine (10 micromol/L) and attenuated by the XOR inhibitor allopurinol (100 micromol/L) in acidic and

129 Importantly, the XOR inhibitors allopurinol and oxypurinol attenuate dysf

130 f the 16 possible logic gates, including the XOR gate, by variation of biochemical parameters.

131 The expression of the XOR in humans is strikingly lower than in mice, and both

132 and BTN1A1 null mice showed that most of the XOR in mice lacking BTN1A1 was released from the MFGM in

133 ed with wild-type mice, in which most of the XOR remained membrane-bound.

134 and RBCs was enhanced in the presence of the XOR substrate xanthine (10 micromol/L) and attenuated by

135 Specifically, the XOR function allows the network to respond to either one

136 The solution to the XOR problem is interesting in that it requires only two

137 tein, in milk fat droplet secretion and thus XOR provides another example of "gene sharing".

138 Thus, XOR and eNOS are ideally situated on the membranes of RB

139 Thus, XOR catalyzed nitrate reduction to nitrite and NO occurs

140 As expected, these animals lack tissue XOR activity and have low to undetectable serum levels o

141 ophilin, a membrane protein known to bind to XOR, was clustered at the point of contact of the cytopl

142 the major sources of ROS, we tested whether XOR inhibition could improve cardiac performance and ind

143 To help determine the mechanism by which XOR is regulated, we examined the expression and localiz