ライフサイエンスコーパス: aquaporin 4

1 NMO-IgG reacts with the water channel aquaporin 4.

2 toantibodies against astrocyte water channel aquaporin-4.

3 dies against the glial water channel protein aquaporin-4.

4 olecular target of NMO-IgG was identified as aquaporin-4.

5 0.3) in mice lacking the glial water channel aquaporin-4.

6 -null mouse which lacks sarcolemmal nNOS and aquaporin-4.

7 ting its effect via the perivascular pool of aquaporin-4.

8 as LGI1, N-methyl-D-aspartate receptor, and aquaporin-4.

9 against the astrocytic water channel protein aquaporin-4.

10 tiedema effects via the perivascular pool of aquaporin-4, 2) hypertonic saline attenuates blood-brain

11 sociated with astrocytic proteins, including aquaporin 4, actin, and glutamine synthetase and serine

12 eally injected NMO-IgG binds mouse placental aquaporin-4, activates coinjected human complement, and

13 synthetase, glutamate transporter 1 (GLT1), aquaporin-4, aldehyde dehydrogenase 1 family member L1,

14 and 3) deletion of the perivascular pool of aquaporin-4 alleviates tissue damage after stroke, in mi

15 known to modulate edema formation, including aquaporin-4 and AMP-activated protein kinase and its dow

16 R/MYOC overexpression, including homologs of aquaporin-4 and cytochrome-P450, previously associated w

17 also trigger an autoimmune reaction against aquaporin-4 and inflammation of the CNS.

18 tic and expressed increased levels of water (aquaporin-4) and ion (Kir4.1) channels.

19 on depending on the presence of perivascular aquaporin-4, and 3) deletion of the perivascular pool of

20 luding eight sites among aquaporin-2 (AQP2), aquaporin-4, and urea transporter isoforms A1 and A3.

21 ic neuritis and myelitis and the presence of aquaporin 4 antibodies (AQP4-abs).

22 Testing for aquaporin 4 antibodies was undertaken in all suspected c

23 Aquaporin 4 antibodies were tested using 2 sensitive ass

24 Patients with neuromyelitis optica who have aquaporin-4 antibodies are being identified and receivin

25 rtunistic retinal infection in patients with aquaporin-4 antibodies who are receiving immunosuppressa

26 nistic infections can occur in patients with aquaporin-4 antibodies who are receiving relatively low

27 We describe 2 patients with aquaporin-4 antibodies who were receiving conventional d

28 Aquaporin 4 antibody (AQP4-Ab)-negative patients with lo

29 sability Status Scale score), change in anti-aquaporin 4 antibody, and safety of rituximab treatment.

30 Aquaporin 4 antibody-negative neuromyelitis optica (NMO)

31 come, and prognostic features in relation to Aquaporin-4 antibody (AQP4-Ab) status, and compared to a

32 etrospective observational case series of 14 aquaporin-4 antibody positive NMO and NMO spectrum disor

33 O according to Wingerchuk's 2006 criteria or aquaporin-4 antibody-positive NMO spectrum disorder (NMO

34 We report 12 aquaporin-4 antibody-positive patients (12% of seroposit

35 tcomes and prognostic characteristics of 106 aquaporin-4 antibody-seropositive patients from the UK a

36 (1) Retrospective cohort of 76 aquaporin 4-antibody (AQP4-Ab)-positive patients from Ox

37 METHOD: (1) Retrospective cohort of 76 aquaporin 4-antibody (AQP4-Ab)-positive patients from Ox

38 Aquaporin 4 (AQ4) is not expressed in the choroid plexus

39 against the astrocyte water channel protein aquaporin 4 (AQP4) and the evidence that AQP4-IgG is inv

40 cooperation between the glial water channel aquaporin 4 (AQP4) and the transient receptor potential

41 Aquaporin 4 (AQP4) appeared distributed all over the cel

42 neuritis (ON), the presence of antibodies to aquaporin 4 (AQP4) has diagnostic and prognostic value.

43 d protein) and supramolecular aggregation of aquaporin 4 (AQP4) in mouse, rat, and human tissues.

44 staining showed aberrant co-localization of aquaporin 4 (AQP4) in retracted GFAP+ astrocytes with di

45 Aquaporin 4 (AQP4) is highly expressed at perivascular g

46 Aquaporin 4 (AQP4) is highly expressed in the glial cell

47 tion after binding of an IgG autoantibody to aquaporin 4 (AQP4) is thought to be a major determinant

48 Water channel aquaporin 4 (AQP4) plays a key role in the regulation of

49 ostasis.SIGNIFICANCE STATEMENT Water channel aquaporin 4 (AQP4) plays a key role in the regulation of

50 Moreover, mRNA expression of water channel, aquaporin 4 (AQP4) was increased after Dp71 deletion.

51 receptor potential isoform 4 (TRPV4) and the aquaporin 4 (AQP4) water channel in retinal Muller cells

52 brain to edema formation by up-regulation of aquaporin 4 (AQP4), a water channel in the brain that ha

53 Aquaporins, particularly aquaporin 4 (Aqp4), are membrane proteins with important

54 tion of an astrocytic water channel protein, Aquaporin 4 (AQP4), is known to predominantly contribute

55 f the perivascular pool of the water channel aquaporin 4 (AQP4), suggesting that an efficient clearan

56 Aquaporin 4 (AQP4)-specific autoantibodies in neuromyeli

57 2) and the astrocyte-specific water channel, aquaporin 4 (AQP4).

58 e expression of the astrocytic water channel aquaporin-4 (AQP4) and changes in glymphatic pathway fun

59 In adult retina, aquaporin-4 (AQP4) and inwardly rectifying K(+) (Kir4.1)

60 onally, loss of astrocytic laminin decreases aquaporin-4 (AQP4) and tight junction protein expression

61 However, since the discovery of NMO-IgG or aquaporin-4 (AQP4) antibody (AQP4-antibody), an NMO-spec

62 toantibodies against astrocyte water channel aquaporin-4 (AQP4) are highly specific for the neuroinfl

63 toantibodies against astrocyte water channel aquaporin-4 (AQP4) are thought to be pathogenic in neuro

64 M23" isoform of the glial cell water channel aquaporin-4 (AQP4) assembles into orthogonal arrays of p

65 ral nervous system caused by binding of anti-aquaporin-4 (AQP4) autoantibodies (NMO-IgG) to AQP4 on a

66 ogy compatible with targeting of sarcolemmal aquaporin-4 (AQP4) by complement-activating IgG implies

67 Aquaporin-4 (AQP4) can assemble into supramolecular aggr

68 bulin [Ig]G) against astrocyte water channel aquaporin-4 (AQP4) cause complement- and cell-mediated a

69 ogenic autoantibodies (NMO-IgG) to astrocyte aquaporin-4 (AQP4) causes complement-dependent cytotoxic

70 Aquaporin-4 (AQP4) deficiency in mice reduces neuroinfla

71 Aquaporin-4 (AQP4) deletion slowed K(+) reuptake about t

72 was no significant alteration in ipsilateral Aquaporin-4 (AQP4) expression following MCAO or progeste

73 Perivascular localization of aquaporin-4 (AQP4) facilitates the clearance of intersti

74 The astroglial water channel aquaporin-4 (AQP4) facilitates water movement into and o

75 ress the mercurial-insensitive water channel aquaporin-4 (AQP4) for purification and reconstitution.

76 The water channel aquaporin-4 (AQP4) forms supramolecular clusters whose s

77 The aquaporin-4 (AQP4) gene encodes proteins of approximatel

78 Two major isoforms of aquaporin-4 (AQP4) have been described in human tissue.

79 rin-1 (AQP1) in microvascular endothelia and aquaporin-4 (AQP4) in airway epithelia.

80 The organization of aquaporin-4 (AQP4) into large plasma membrane assemblies

81 Aquaporin-4 (AQP4) is a mercurial-insensitive, water-sel

82 Aquaporin-4 (AQP4) is a primary influx route for water d

83 Aquaporin-4 (AQP4) is a water channel protein expressed

84 Aquaporin-4 (AQP4) is a water transport protein expresse

85 Aquaporin-4 (AQP4) is a water-selective transport protei

86 Aquaporin-4 (AQP4) is enriched at the sarcolemma of skel

87 The astrocyte water channel aquaporin-4 (AQP4) is expressed as heterotetramers of M1

88 Aquaporin-4 (AQP4) is found on the basolateral plasma me

89 Aquaporin-4 (AQP4) is the major water channel expressed

90 Aquaporin-4 (AQP4) is the major water channel in the bra

91 Aquaporin-4 (AQP4) is the major water channel in the CNS

92 Aquaporin-4 (AQP4) is the primary water channel in the m

93 eposition, as well as an astrocytopathy with aquaporin-4 (AQP4) loss.

94 Using an aquaporin-4 (AQP4) M1-isoform-specific enzyme-linked imm

95 the brain involves movement of water through aquaporin-4 (AQP4) membrane channels.

96 sts that the Muller/glial cell water channel aquaporin-4 (AQP4) modulates K(+) channel function of th

97 toantibodies (NMO-immunoglobulin G [IgG]) to aquaporin-4 (AQP4) on astrocytes, which initiates comple

98 cytic processes (labeled with antibodies for aquaporin-4 (AQP4) or glial fibrillary acidic protein we

99 ular localization of the brain water channel aquaporin-4 (AQP4) was investigated during the neurologi

100 biogenesis, hydrophilic peptide loops of the aquaporin-4 (AQP4) water channel are delivered to cytoso

101 The Aquaporin-4 (AQP4) water channel contributes to brain wa

102 The astrocytic aquaporin-4 (AQP4) water channel is the target of pathog

103 toantibodies (NMO-IgGs) directed against the aquaporin-4 (AQP4) water channel located on astrocyte fo

104 Aquaporin-4 (AQP4) water channel-specific IgG distinguis

105 Here, we examined the role of aquaporin-4 (AQP4) water channels after experimental con

106 Aquaporin-4 (AQP4) water channels are expressed strongly

107 re electron microscopy (FFEM) indicates that aquaporin-4 (AQP4) water channels can assemble in cell p

108 earance mechanism additionally suggests that aquaporin-4 (AQP4) water channels facilitate convective

109 Tetramers of aquaporin-4 (AQP4) water channels form supramolecular as

110 s optica-immunoglobulin G (NMO-IgG) binds to aquaporin-4 (AQP4) water channels in the central nervous

111 The plasma membrane assembly of aquaporin-4 (AQP4) water channels into orthogonal arrays

112 This autoantibody targets astrocytic aquaporin-4 (AQP4) water channels.

113 Here we show that mice deficient in aquaporin-4 (AQP4), a glial membrane water channel, have

114 Aquaporin-4 (AQP4), a water channel expressed in astrocy

115 ous studies have reported an upregulation of aquaporin-4 (AQP4), a water channel protein, following b

116 MO patients carry IgG autoantibodies against aquaporin-4 (AQP4), an astrocytic water channel.

117 fusion in the ECS was faster in mice lacking aquaporin-4 (AQP4), an astroglial water channel that fac

118 Determination of antibodies to NMDAR, aquaporin-4 (AQP4), and myelin oligodendrocyte glycoprot

119 e-specific major water channel in the brain, aquaporin-4 (AQP4), in brain plasticity and learning.

120 -IgGs) against supra-molecular assemblies of aquaporin-4 (AQP4), known as orthogonal array of particl

121 Subsequently, aquaporin-4 (AQP4), the most abundant water channel in t

122 rum autoantibody biomarker, NMO-IgG, targets aquaporin-4 (AQP4), the most abundant water channel prot

123 Aquaporin-4 (AQP4), the primary water channel in glial c

124 Aquaporin-4 (AQP4), the principal water channel in astro

125 he extent of a brain-specific water channel, aquaporin-4 (AQP4), using confocal and electron microsco

126 e discovery of serum antibodies (Ab) against aquaporin-4 (AQP4), which unequivocally differentiate NM

127 isation of GABA(A) receptors (GABA(A)Rs) and aquaporin-4 (AQP4)-containing protein complexes in neuro

128 ord MRIs for ring-enhancing lesions from 284 aquaporin-4 (AQP4)-IgG seropositive patients at Mayo Cli

129 ptic neuritis, multiple sclerosis (MS), anti-aquaporin-4 (AQP4)-negative neuromyelitis optica (NMO),

130 Aquaporin-4 (AQP4)-specific T cells are expanded in neur

131 c autoantibodies (NMO-IgG) against astrocyte aquaporin-4 (AQP4).

132 against the astrocyte water channel protein aquaporin-4 (AQP4).

133 lin G [IgG]) against astrocyte water channel aquaporin-4 (AQP4).

134 er fluxes augmented by vasopressin-regulated aquaporin-4 (AQP4).

135 ibodies (NMO-IgG) to astrocyte water channel aquaporin-4 (AQP4).

136 pectrum disorder have autoantibodies against aquaporin-4 (AQP4-Abs), but recently, myelin-oligodendro

137 The discovery of aquaporin-4 as the putative target of NMO-IgG, and recen

138 GFAP-aquaporin 4 association decreased during initial sucklin

139 reduced and then increased the expression of aquaporin 4, astrocytic water channels coupled to K(+) c

140 t the Delta PDZ form, reestablished nNOS and aquaporin-4 at the sarcolemma of these mice.

141 e investigated whether immunoglobulin G from aquaporin-4-autoantibody-positive neuromyelitis optica p

142 ing in the setting of neoplasia suggest that aquaporin-4 autoimmunity may in some cases have a parane

143 athogenic IgG that competes with NMO-IgG for aquaporin-4 binding, significantly reduced NMO-IgG and h

144 cyclinD1, fibulin 2, tenascin C, TIMP1, and aquaporin-4, correlations were significantly nonlinear,

145 rted previously that astroglia cultured from aquaporin-4-deficient (AQP4-/-) mice migrate more slowly

146 Data suggest that autoantibodies to aquaporin 4 derived from peripheral B cells cause the ac

147 mportant in determining clinical outcomes in aquaporin-4 disease.

148 hich recognize the immunodominant epitope of aquaporin-4, exhibit Th17 polarization and cross-react w

149 This is associated with increased aquaporin 4 expression in the intestinal mucosa and subm

150 At a molecular level, aquaporin-4 expression decreased and the expression and

151 Placental aquaporin-4 expression is high during mid-gestation and

152 man complement, there was a striking loss of aquaporin-4 expression, glial cell oedema, myelin breakd

153 components, extensive demyelination, loss of aquaporin-4 expression, loss of reactive astrocytes and

154 This is associated with up-regulation of aquaporin 4 gene expression and protein.

155 dy responses to the astrocytic water channel aquaporin 4 have been described.

156 OSD whose test results were seropositive for aquaporin-4 IgG and who had a hepatic metastasis from a

157 icrocystic changes in terms of age, sex, and aquaporin 4-IgG antibody status.

158 ange, 13-81 years); 84% were women; 80% were aquaporin 4-IgG seropositive; and the median Expanded Di

159 n both N-methyl-D-aspartate receptor-IgG and aquaporin-4-IgG coexisted (71%).

160 ence (on December 31, 2011) of NMO/NMOSD and aquaporin-4-IgG seroincidence and seroprevalence (sera c

161 idemiological studies are limited by lack of aquaporin-4-IgG seroprevalence assessment, absence of po

162 Aquaporin-4-IgG was measured by M1-isoform-fluorescent-a

163 ng diseases (IDD) with a specific biomarker, aquaporin-4-IgG.

164 ysed using cell-based assays for MOG-IgG and aquaporin-4 immunoglobulin G (AQP4-IgG).

165 All NMOSD patients were positive for aquaporin-4-immunoglobulin G, and all sarcoidosis cases

166 The tumor cells expressed aquaporin-4 immunoreactivity.

167 mmunopathologic studies suggest that loss of aquaporin-4 immunostaining is detectable in early lesion

168 markers, glial fibrillary acidic protein and aquaporin-4 immunostaining) at both time periods postisc

169 ein expression of the water channel protein, aquaporin 4 in these mice.

170 dicates that the autoimmune response against aquaporin-4 in neuromyelitis optica may be triggered by

171 ganization of the blood-brain barrier marker aquaporin-4 in the optic nerves were observed during the

172 otoxicity (ADCC) in cell cultures expressing aquaporin-4 in the presence of NMO autoantibody (NMO-IgG

173 hat the sarcolemmal localization of nNOS and aquaporin-4 in vivo depends on the presence of a dystrop

174 as no damage to maternal organs that express aquaporin-4, including the brain, spinal cord, kidneys,

175 Aquaporin-4 is a mammalian water channel protein that is

176 Aquaporin-4 is abundant in brain and probably participat

177 In this study, we show that aquaporin-4 is expressed in the syncytiotrophoblast of h

178 al features of neuromyelitis optica and that aquaporin-4 is necessary and sufficient for immunoglobul

179 tex in wild-type mice and 0.211 +/- 0.003 in Aquaporin-4 knockout mice.

180 Aquaporin 4 may be a useful therapeutic target for strat

181 nt, non-NMO-IgG with human complement, or in aquaporin-4 null mice injected with NMO-IgG and human co

182 optica patients with human complement, or in aquaporin-4-null mice that received immunoglobulin G fro

183 totic, express glutamate receptors, and form aquaporin-4(+) perivascular endfeet.

184 localization of the astrocytic water channel aquaporin 4 persisted long after injury, recovering only

185 t of cerebral edema; 2) perivascular pool of aquaporin-4 plays a critical role in water egress from b

186 (alpha-Syn(-/-)) that lack the perivascular aquaporin-4 pool but retain the endothelial pool of this

187 yn) that demonstrate diminished perivascular aquaporin-4 pool but retain the non-endfoot and ependyma

188 lux of water from brain via the perivascular aquaporin-4 pool.

189 od-brain barrier disruption via perivascular aquaporin-4 pool.

190 ian age of 39 years (range, 26-40 years) and aquaporin 4-positive NMO.

191 Total aquaporin-4 protein expression was not different between

192 content, blood-brain barrier disruption, and aquaporin-4 protein expression were determined at 24 hou

193 Pregnancy-induced up-regulation of aquaporin-4 protein in brain and its role in eclampsia.

194 by a self-reactive Ab against the astrocyte aquaporin-4 protein.

195 vity between bacterial aquaporin-Z and human aquaporin-4 proteins.

196 Labeling with the gliovascular marker aquaporin-4 revealed that at least half of the TH cells

197 ic and neuroimaging observations suggest the aquaporin-4-rich area postrema may be a first point of a

198 A patient with highly active aquaporin 4-seropositive NMO who failed numerous immunos

199 of NMO-IgG, and recent data suggesting that aquaporin-4-specific antibodies are pathogenic may enhan

200 s, an IgG autoantibody binding to astrocytic aquaporin 4, the principal water channel of the central

201 iated with the disease-specific autoantibody aquaporin-4, thought to be pathogenic.

202 arget antigens included CASPR2, LGI1, NMDAR, aquaporin 4, Tr (DNER [delta/notch-like epidermal growth

203 Less frequent were aquaporin-4, voltage-gated Kv1 potassium channel-complex

204 oss-immunoreactivity between aquaporin-Z and aquaporin-4 was investigated and ascertained in multiple

205 store sarcolemmal nNOS (although sarcolemmal aquaporin-4 was restored).

206 al fibrillary acidic protein (GFAP), or with aquaporin 4, was found in perivascular astrocytes of cor

207 abnormalities to be associated with loss of aquaporin-4 water and Kir4.1 potassium channels from gli

208 Aquaporin-4 water channel gene deletion caused significa

209 e show that NMO-IgG binds selectively to the aquaporin-4 water channel, a component of the dystroglyc

210 s (neuromyelitis optica) a serum antibody to aquaporin-4 water channels has been detected.

211 e, neuronal nitric oxide synthase (nNOS) and aquaporin-4 were absent from the sarcolemma.

212 etiformis and antibody test findings against aquaporin-4 were positive, leading to a diagnosis of neu

213 e gene encoding the astroglial water channel aquaporin-4, which is importantly involved in paravascul

214 This biomarker targets the water channel aquaporin-4, which is lost in neuromyelitis optica lesio