ライフサイエンスコーパス: AQP4

1 P4) and large orthogonal arrays of AQP4 (M23-AQP4).

2 nd mislocalization of astrocyte aquaporin-4 (AQP4).

3 ; glycine receptors (GLY-R); water channels (AQP4).

4 ies targeting the aquaporin-4 water channel (AQP4).

5 nnel in Xenopus laevis oocytes together with AQP4.

6 est that NH3 is able to permeate the pore of AQP4.

7 n levels and water permeability to wild-type AQP4.

8 ting that the ionic NH4 (+) did not permeate AQP4.

9 ytes, TRPV4 activation became independent of AQP4.

10 ptides from various myelin proteins and from AQP4.

11 ave reported an upregulation of aquaporin-4 (AQP4), a water channel protein, following brain injury.

12 n patients with NMOSD (n=39, 28 aquaporin-4 (AQP4)-Ab-seropositive, 3 double-Ab-seronegative, 4 myeli

13 -1.1 yrs) for AQP4-Ab positive vs 2.4 yrs in AQP4-Ab negative cases (95% CI 1.1-3.6 yrs).

14 a national cohort sample of known sequential AQP4-Ab negative first episode CNS acquired demyelinatio

15 Since patients with AQP4-Ab negative NMO/SD require different management, th

16 yelination cases (n = 29; females = 55%; all AQP4-Ab negative; median age = 13.6 yrs).

17 sing-remitting multiple sclerosis (RRMS) and AQP4-ab NMOSD patients and also assessed their value in

18 0.9% and with a specificity of 87.1% against AQP4-ab NMOSD, 95.2% against MOG-ab NMOSD and 87.5% in t

19 Twenty NMO cases (females = 90%; AQP4-Ab positive = 60%; median age = 10.5 yrs) with medi

20 relapse = 0.76 yrs (95% CI 0.43-1.1 yrs) for AQP4-Ab positive vs 2.4 yrs in AQP4-Ab negative cases (9

21 phenotype and the highly specific assays, 66 AQP4-Ab seropositive samples were used to establish the

22 Early AQP4-Ab testing may allow prompt immunomodulatory treatm

23 The AQP4-ab titers (P = .02) and pain levels (P = .02) dropp

24 icentre study of aquaporin (AQP) 4 antibody (AQP4-Ab) assays in neuromyelitis optica spectrum disorde

25 eatures in relation to Aquaporin-4 antibody (AQP4-Ab) status, and compared to a non NMO control cohor

26 ospective cohort of 76 aquaporin 4-antibody (AQP4-Ab)-positive patients from Oxford and Liverpool's n

27 ospective cohort of 76 aquaporin 4-antibody (AQP4-Ab)-positive patients from Oxford and Liverpool's n

28 es, encephalitis, anti-aquaporin-4-antibody (AQP4-Ab)-seronegative neuromyelitis optica spectrum diso

29 MOG-Ab-associated disease is different to AQP4-Ab-positive NMOSD and MS.

30 (2) Focused prospective study of 26 AQP4-Ab-positive Oxford patients, a subset of the retros

31 dally located (ie, thoracic) cord lesions in AQP4-Ab-positive patients associate with high postmyelit

32 112 patients with NMOSD (31 AQP4-ab-positive, 21 MOG-ab-positive, 16 ab-negative) or

33 yte glycoprotein (MOG)-Ab-seropositive and 4 AQP4-Ab-seronegative with unknown MOG-Ab-serostatus), mu

34 s of white race/ethnicity with highly active AQP4-ab-seropositive NMO (n = 6) and NMO spectrum disord

35 ly correlated, particularly in patients with AQP4-Ab-seropositive NMOSD (r(s)=0.70, p<0.001).

36 imilar pattern of elevation in patients with AQP4-Ab-seropositive NMOSD.

37 Patients who test positive for AQP4-Abs and present with optic neuritis (ON) and transv

38 and the presence of aquaporin 4 antibodies (AQP4-abs).

39 channel activities of AQP1 but did not alter AQP4 activity, whereas bacopaside II selectively blocked

40 This study demonstrates how AQP4 aggregation influences plasma membrane dynamics to

41 The role of AQP4 aggregation into OAP in malignant gliomas is still

42 The isoform ratio controls AQP4 aggregation into supramolecular structures called o

43 y potentiate invasiveness potential, whereas AQP4 aggregation may activate the apoptotic path.

44 In conclusion, this study demonstrates that AQP4 aggregation state might be an important determinant

45 ily associated with edema formation but with AQP4 aggregation/disaggregation dynamics and their link

46 In this study, we demonstrate that AQP4 aggregation/disaggregation into OAP influences the

47 Imaging secondary antibodies bound to M1-AQP4 allowed us to infer the size of individual AQP4-IgG

48 AD by Western blot or immunofluorescence for AQP4, amyloid-beta 1-42, and glial fibrillary acidic pro

49 arry IgG autoantibodies against aquaporin-4 (AQP4), an astrocytic water channel.

50 itutions in the selectivity filters of AQP1, AQP4 and AQP3 differentially affect glycerol and urea pe

51 mbrane analog, also causes the clustering of AQP4 and beta-DG.

52 o noted strikingly similar redistribution of AQP4 and GFAP+ astrocytes transformed into clasmatodendr

53 gh delocalization and down-regulation of the AQP4 and Kir4.1 channels (1).

54 lial end foot, which regulates expression of Aqp4 and Kir4.1 genes and facilitates the time course an

55 amers in the plasma membrane made of the M23-AQP4 and M1-AQP4 isoforms.

56 rsors, which were tested for both binding to AQP4 and poly- or autoreactivity.

57 y mismatch between the hydrophobic length of AQP4 and the bilayer hydrocarbon thickness, could explai

58 of TRPV4 did not affect the distribution of AQP4 and vice versa.

59 specificity bound to isolated tetramers (M1-AQP4) and large orthogonal arrays of AQP4 (M23-AQP4).

60 between the glial water channel aquaporin 4 (AQP4) and the transient receptor potential isoform 4 (TR

61 vides an opportunity to image membrane-bound AQP4 antibodies (AQP4-IgG) and evaluate changes in their

62 ith MOG antibodies and 12 of 13 (92.5%) with AQP4 antibodies (p < 0.001).

63 We found that human AQP4 antibodies caused acute astrocyte depletion with in

64 odies, 4 (8%) had MOG antibodies, 2 (4%) had AQP4 antibodies concurrent with MOG antibodies, and 5 (1

65 Patients with AQP4 antibodies had the poorest visual outcomes, whereas

66 rimental NMO-related lesions caused by human AQP4 antibodies in mice.

67 pectively studied adult patients with MOG or AQP4 antibodies who received RTX under an individualized

68 lly if biomarker testing (such as serum anti-AQP4 antibodies) is not informative.

69 rols with neuromyelitis optica, 37 (77%) had AQP4 antibodies, 4 (8%) had MOG antibodies, 2 (4%) had A

70 16 patients with MOG antibodies and 29 with AQP4 antibodies, mean follow-up was 19 (range = 9-38) an

71 odies, and 13 occurred in 7 of 29 (24%) with AQP4 antibodies.

72 etween MOG antibody oligodendrocytopathy and AQP4 antibody astrocytopathy suggests that the primary i

73 e toxicity and axon damage were dependent on AQP4 antibody concentration and complement, specifically

74 and 18 children) with MOG antibody (n = 26), AQP4 antibody disease (n = 26) and multiple sclerosis (n

75 riminated from MOG antibody disease and from AQP4 antibody disease with high predictive values, while

76 e could not be accurately discriminated from AQP4 antibody disease.

77 from multiple sclerosis but overlapped with AQP4 antibody disease.

78 differ from those of multiple sclerosis and AQP4 antibody disease.

79 In AQP4 antibody-associated disorder, relapse mostly occurs

80 t of NMO-related acute axon injury following AQP4 antibody-mediated astrocyte depletion.

81 ve expression of the OAP-forming isoform M23-AQP4 (AQP4-OAP) triggered cell shape changes in glioma c

82 By contrast, expression of M1-AQP4 (AQP4-tetramers), which is unable to aggregate into

83 nted in vitro following IgG interaction with AQP4: AQP4 internalization, attenuated glutamate uptake,

84 ogical outcomes of IgG binding to astrocytic AQP4 are poorly understood.

85 assembly of larger AQP4-IgG complexes on M23-AQP4 arrays.

86 specific patterns of bound antibodies on M23-AQP4 arrays.

87 esterol-containing lipid bilayer, suggesting AQP4 as a favored transmembrane route for NH3 Our data p

88 utoreactive, suggesting that pathogenic anti-AQP4 autoantibodies can originate from the pool of autor

89 next explored whether pathogenic NMOSD anti-AQP4 autoantibodies can originate from the pool of poly-

90 Six human anti-AQP4 autoantibodies that acquired somatic mutations were

91 ation is required for the generation of anti-AQP4 autoantibodies.

92 membrane route for NH3 Our data propose that AQP4 belongs to the growing list of NH3-permeable water

93 AQP4 blockade altered T cell gene and protein expression

94 pressed by naive and memory T cells and that AQP4 blockade with a small molecule inhibitor prolongs m

95 monstrate that AQP4 internalization requires AQP4-bound IgG to engage an astrocytic Fcgamma receptor

96 T cells specific for either determinant from AQP4(-/-), but not WT, mice induced paralysis in recipie

97 Antibodies against AQP4 can damage astrocytes via complement, but NMO histo

98 Calmodulin directly binds the AQP4 carboxyl terminus, causing a specific conformationa

99 Here we show that AQP4 cell surface expression can be rapidly and reversib

100 Here we show that AQP4 cell-surface abundance increases in response to hyp

101 a specific conformational change and driving AQP4 cell-surface localization.

102 ent and MD-simulation results indicated that AQP4 channel permeability decreased with decreasing bila

103 the incorporation of additional cytoplasmic AQP4 channels and the redistribution of AQP4 channels of

104 smic AQP4 channels and the redistribution of AQP4 channels of the existing OAPs; and AQP4e affects th

105 araffin sections of brain tissue and support AQP4 cluster size as a primary determinant of its subcel

106 g demonstrated colocalization of Kir4.1 with AQP4 clusters in perivascular areas but not in parenchym

107 ng size-dependent subcellular segregation of AQP4 clusters.

108 ed energy barrier for NH3 permeation through AQP4 compared with that of a cholesterol-containing lipi

109 Interaction of the IgG-AQP4 complex with FcgammaRs triggers coendocytosis of th

110 AQP5 and the isoforms AQP1 and AQP4 decreased, whereas AQP3 increased, levels of plasma

111 ation was observed following immunization of AQP4-deficient (AQP4(-/-)) mice with AQP4 peptide (p) 13

112 d in Aqp4-knockout mice, suggesting that the AQP4-dependent glymphatic system is actively involved in

113 delineated in mice mechanisms that included AQP4-dependent transient astrocytic volume changes and a

114 ts have shown that the water permeability of AQP4 depends on the cholesterol content in the lipid bil

115 AQP4 disaggregation may potentiate invasiveness potentia

116 reactive gliosis and polarized aquaporin-4 (AQP4) distribution.

117 Specifically, water influx through AQP4 drives calcium influx via TRPV4 in the glial end fo

118 is highest during the rest phase and loss of AQP4 eliminates the day-night difference in both glympha

119 However, AQP4 endocytosis requires an activating FcgammaR's gamma

120 tor repertoires for recognition of these two AQP4 epitopes.

121 se caused by antibodies against aquaporin-4 (AQP4) expressed on astrocytes.

122 ar alkalization (or lesser acidification) of AQP4-expressing oocytes, these data suggest that NH3 is

123 Here we observe that AQP4-expressing Xenopus oocytes display a reflection coe

124 pileptic drug that has been shown to inhibit AQP4 expression and in this study we investigate the dru

125 foveal thinning reflected the topography of AQP4 expression and Muller glial distribution in the hum

126 Topography of AQP4 expression and Muller glial distribution were analy

127 Levels of AQP4 expression at different retinal regions.

128 To determine whether alterations in AQP4 expression or loss of perivascular AQP4 localizatio

129 In this study, altered AQP4 expression was associated with aging brains.

130 AQP4 expression was increased in white matter around lat

131 AQP4 expression was significantly increased 24 hours aft

132 reduced tight junction proteins, diminished AQP4 expression, and decreased pericyte coverage are res

133 distribution of Muller cells and patterns of AQP4 expression.

134 or NMO-IgG binding and identified regions of AQP4 extracellular structure that may represent prime ta

135 Co-expression with AQP4 facilitated the cell swelling induced by osmotic ch

136 The glymphatic system, that is aquaporin 4 (AQP4) facilitated exchange of CSF with interstitial flui

137 Perivascular localization of aquaporin-4 (AQP4) facilitates the clearance of interstitial solutes,

138 The glial water channel protein aquaporin-4 (AQP4) forms heterotetramers in the plasma membrane made

139 The goal of this study was to determine how AQP4 function impacts T cells in the absence of antigen

140 st after cardiorespiratory arrest; and (iii) Aqp4 gene deletion did not impair transport of fluoresce

141 e microarray, HLA high-resolution typing and AQP4 gene sequencing data to analyze genetic ancestry an

142 No novel or missense variants in the AQP4 gene were found in Mexican patients with NMO or mul

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

144 ring-enhancing lesions from 284 aquaporin-4 (AQP4)-IgG seropositive patients at Mayo Clinic from 1996

145 The AQP4-IgG age and sex-adjusted seroincidence (6.5 vs 0.7/

146 At a population level, AQP4-IgG and MOG-IgG account for 9% of optic neuritis an

147 Sera were tested for AQP4-IgG and MOG-IgG by using a live-cell-based flow cyt

148 ion of the cause of atypical optic neuritis: AQP4-IgG and MOG-IgG.

149 haracterize the spatial arrangement of bound AQP4-IgG antibodies, yielding multiple epitope-specific

150 4 allowed us to infer the size of individual AQP4-IgG binding events.

151 The resulting model of AQP4-IgG CDC provides a framework for understanding clas

152 ion was used to model the assembly of larger AQP4-IgG complexes on M23-AQP4 arrays.

153 o alterations in AQP4 isoform expression and AQP4-IgG epitope specificity.

154 All 3 patients positive for AQP4-IgG had more than 1 optic neuritis attack, 2 with r

155 ic neuritis has a better visual outcome than AQP4-IgG optic neuritis.

156 ts at the Mayo Clinic who were identified as AQP4-IgG positive from 1996 to 2014.

157 was significantly worse in patients who were AQP4-IgG seropositive (p=0.034), but there was no relati

158 Those derived from three anti-AQP4-IgG seropositive NMOSD patients (n = 130) were comp

159 nalysis of our original cohort revealed that AQP4-IgG seropositivity increased from 56% to 75% for NM

160 Inclusion criteria were as follows: (1) AQP4-IgG seropositivity, (2) myelitis attack and (3) MRI

161 e myelitis does not exclude consideration of AQP4-IgG testing or NMOSD diagnosis.

162 ity to image membrane-bound AQP4 antibodies (AQP4-IgG) and evaluate changes in their spatial distribu

163 or MOG-IgG and aquaporin-4 immunoglobulin G (AQP4-IgG).

164 porin-4 (AQP4) water channel autoantibodies (AQP4-IgG).

165 e was significantly reduced in patients with AQP4-IgG+ NMOSD in scotopic ERGs (compared with AQP4-IgG

166 retinal layers at the fovea in patients with AQP4-IgG+ NMOSD, in the Henle fiber outer nuclear layer

167 r glial dysfunction in eyes of patients with AQP4-IgG+ NMOSD.

168 In a subset of patients negative for AQP4-IgG, pathogenetic serum IgG antibodies to myelin ol

169 4-IgG+ NMOSD in scotopic ERGs (compared with AQP4-IgG- subjects, patients with MS, and normal control

170 Although AQP4-IgG-driven complement-dependent cytotoxicity (CDC)

171 spectrum disorder (NMOSD, n=10), idiopathic AQP4-IgG-negative myelitis (n=4), idiopathic AQP4-IgG-ne

172 AQP4-IgG-negative myelitis (n=4), idiopathic AQP4-IgG-negative optic neuritis (n=4), other demyelinat

173 TM than in 27 population-based patients with AQP4-IgG-negative STM included the following: nonwhite r

174 <0.001) but not significantly different from AQP4-IgG-NMOSD (14/30 (47%); p=0.07).

175 al bands were rare in MOGAD (5/30 (17%)) and AQP4-IgG-NMOSD (2/22 (9%); p=0.68) but common in MS (18/

176 /37 (46%)) over MS (3/30 (10%); p=0.001) and AQP4-IgG-NMOSD (3/30 (10%); p=0.001).

177 We compared the symptomatic attacks to AQP4-IgG-NMOSD (n=30) and MS (n=30).

178 ibutes that can help discriminate MOGAD from AQP4-IgG-NMOSD and MS.

179 s younger than MS at 36 (16-65; p=0.046) and AQP4-IgG-NMOSD at 45 (6-72; p=0.006).

180 I lesions occasionally occurred in MOGAD and AQP4-IgG-NMOSD but never in MS.

181 ies, have been approved for the treatment of AQP4-IgG-positive NMO and its formes frustes.

182 Attributes more common in patients with AQP4-IgG-positive STM than in 27 population-based patien

183 c in 29%, MOG-IgG-associated disorder in 5%, AQP4-IgG-seropositive neuromyelitis optic spectrum disor

184 ed secondary antibody labeling of monoclonal AQP4-IgGs with differing epitope specificity bound to is

185 we assessed the co-localization of GFAP and AQP4 immunoreactivities in post-mortem brains from adult

186 itis revealed tissue vacuolation and loss of AQP4 immunoreactivity with preserved axons.

187 Expression of AQP4 protein, AQP4 immunoreactivity, and perivascular AQP4 localizatio

188 nality in modulating the expression level of AQP4 in an in vitro luciferase reporter assay.

189 study shows a new perspective on the role of AQP4 in brain tumors not necessarily associated with ede

190 on of experiments and simulations to analyze AQP4 in cholesterol-free phospholipid bilayers with simi

191 Native AQP4 in mouse cortex, where both isoforms are expressed,

192 s also suggested structural modifications in AQP4 in response to changes in bilayer thickness.

193 In mouse retinas, TRPV4 colocalized with AQP4 in the end feet and radial processes of Muller astr

194 bsequently, we establish the central role of AQP4 in the glymphatic clearance of tau from the brain;

195 multiple sclerosis (MS) and to aquaporin-4 (AQP4) in neuromyelitis optica spectrum disorders (NMOSDs

196 wed aberrant co-localization of aquaporin 4 (AQP4) in retracted GFAP+ astrocytes with disrupted end-f

197 ealed an increased expression of aquaporin4 (AQP4) in the flight hippocampus compared to the controls

198 jor water channel in the brain, aquaporin-4 (AQP4), in brain plasticity and learning.

199 uninjected oocytes and in oocytes expressing AQP4, indicating that the ionic NH4 (+) did not permeate

200 Consistent with the in vitro data, in vivo AQP4 inhibition reduced T lymphocyte numbers in the lymp

201 AQP4 inhibition transiently reduced the number of circul

202 dies demonstrated T cell intrinsic effect of AQP4 inhibition.

203 ge and tau protein clearance using the novel AQP4 inhibitor, TGN-020.

204 permeability were due to direct cholesterol-AQP4 interactions or to indirect effects caused by chole

205 Here, we demonstrate that AQP4 internalization requires AQP4-bound IgG to engage a

206 n vitro following IgG interaction with AQP4: AQP4 internalization, attenuated glutamate uptake, intra

207 The organization of aquaporin-4 (AQP4) into large plasma membrane assemblies provides an

208 odulin-mediated cell-surface localization of AQP4 is a viable strategy for development of CNS edema t

209 We recently reported that AQP4 is expressed by naive and memory T cells and that A

210 The perivascular polarization of AQP4 is highest during the rest phase and loss of AQP4 e

211 and that the astroglial water transport via AQP4 is involved in tau clearance from the brain interst

212 The water channel protein aquaporin-4 (AQP4) is expressed in astrocytes and mediates water flux

213 Aquaporin 4 (AQP4) is highly expressed at perivascular glia end-feet

214 Aquaporin 4 (AQP4) is highly expressed in the glial cells of the cent

215 ell lines expressing the tetramer-forming M1-AQP4 isoform display higher activity of matrix metallopr

216 r spatial distribution due to alterations in AQP4 isoform expression and AQP4-IgG epitope specificity

217 Glioma cell lines expressing the M23-AQP4 isoform, which forms large aggregates of orthogonal

218 Although several AQP4 isoforms have been identified in the mammalian brai

219 is study provides new insight on the role of AQP4 isoforms in the biology of gliomas.See related arti

220 plasma membrane made of the M23-AQP4 and M1-AQP4 isoforms.

221 In the following experiments, AQP4 knock-down in mice not only impaired hippocampal vo

222 Such beneficial effects were abolished in Aqp4-knockout mice, suggesting that the AQP4-dependent g

223 s in AQP4 expression or loss of perivascular AQP4 localization are features of the aging human brain

224 ein, AQP4 immunoreactivity, and perivascular AQP4 localization in the frontal cortex were evaluated.

225 Loss of perivascular AQP4 localization may be a factor that renders the aging

226 the licensed drug trifluoperazine inhibited AQP4 localization to the blood-spinal cord barrier, abla

227 en controlling for age, loss of perivascular AQP4 localization was associated with increased amyloid-

228 Perivascular AQP4 localization was significantly associated with AD s

229 supported by the water channel aquaporin-4 (AQP4) localized to vascular endfeet of astrocytes.

230 A network of AQP4 loop D hydrogen bonding interactions, identified us

231 MO-IgG alone caused astrocyte activation and AQP4 loss.

232 ers (M1-AQP4) and large orthogonal arrays of AQP4 (M23-AQP4).

233 ive cell-based assays (CBA) for aquaporin-4 (AQP4)-M23-IgG and myelin-oligodendrocyte glycoprotein (M

234 lthough the proposed requirement for a TRPV4-AQP4 macromolecular complex remains to be resolved.

235 The channel (unit) water permeabilities of AQP4 measured by osmotic-gradient experiments were 3.5 +

236 at laminin111 appears to negatively regulate AQP4-mediated water transport in astrocytes, suppressing

237 In comparison with WT mice, AQP4(-/-) mice used unique T-cell receptor repertoires f

238 ed following immunization of AQP4-deficient (AQP4(-/-)) mice with AQP4 peptide (p) 135-153 or p201-22

239 We determined the presence of antibodies to AQP4, MOG, and GlyR using cell-based assays.

240 Non-tetrameric AQP4 mutants are unable to relocalize to the plasma memb

241 as osmotically matched for AQP4-positive and AQP4-negative oocytes, TRPV4 activation became independe

242 ationship between the actin cytoskeleton and AQP4-OAP and AQP4-tetramers.

243 ression of the OAP-forming isoform M23-AQP4 (AQP4-OAP) triggered cell shape changes in glioma cells a

244 tures called orthogonal arrays of particles (AQP4-OAP).

245 formed organized clusters on supramolecular AQP4 orthogonal arrays, linking epitope-dependent multim

246 Fine mapping of AQP4 p201-220 and p135-153 epitopes identified peptides

247 tion of AQP4-deficient (AQP4(-/-)) mice with AQP4 peptide (p) 135-153 or p201-220, peptides predicted

248 Water channel aquaporin 4 (AQP4) plays a key role in the regulation of water homeos

249 FICANCE STATEMENT Water channel aquaporin 4 (AQP4) plays a key role in the regulation of water homeos

250 onfirmed by alleviation of the impairment of AQP4 polarity and accumulation of p-tau in the contralat

251 results suggest that regional disruption of AQP4 polarity following TBI may reduce the clearance of

252 we demonstrate impaired CSF-ISF exchange and AQP4 polarization in a mouse model of tauopathy, suggest

253 the activation of astrocytes and protect the AQP4 polarization in the affected brain region after Abe

254 Here, we show that AQP4 polarization in the perivascular astrocytic end fee

255 he swelling rate was osmotically matched for AQP4-positive and AQP4-negative oocytes, TRPV4 activatio

256 antibody to the extracellular domains of the AQP4 protein and that recombinant IgG (rAb) derived from

257 Expression of AQP4 protein, AQP4 immunoreactivity, and perivascular AQ

258 Targeted mutations of AQP4 rAb Fc domains that enhance or diminish C1q binding

259 y Fc-Fc interaction inhibited CDC induced by AQP4 rAbs and polyclonal NMO patient sera.

260 We identified a group of AQP4 rAbs targeting a distinct extracellular loop C epit

261 Super-resolution microscopy revealed that AQP4 rAbs with enhanced CDC preferentially formed organi

262 ng recombinant AQP4-specific autoantibodies (AQP4 rAbs) derived from affected patients.

263 he affinity of mature autoantibodies against AQP4 ranged from modest to strong (Kd 15.2-559 nM), none

264 be relevant to understanding development of AQP4-reactive T cells in NMO.

265 s to an intracellular loop (loop D) of human AQP4 reduce oligomerization.

266 vertants displayed any detectable binding to AQP4, revealing that somatic hypermutation is required f

267 Our findings indicate that blocking AQP4 reversibly alters T lymphocyte trafficking pattern.

268 Glial cells lacking TRPV4 but not AQP4 showed deficits in hypotonic swelling and regulator

269 tified the most prevalent genetic variant of AQP4 (single nucleotide polymorphism of rs162008 with C

270 Aquaporin-4 (AQP4)-specific T cells are expanded in neuromyelitis opt

271 Binding of AQP4-specific antibodies (NMO-IgG) triggers activation o

272 minants driving CDC in NMO using recombinant AQP4-specific autoantibodies (AQP4 rAbs) derived from af

273 results provide a foundation to evaluate how AQP4-specific T cells contribute to AQP4-targeted CNS au

274 oimmunity (ATCA) and suggest that pathogenic AQP4-specific T-cell responses are normally restrained b

275 AQP4-specific Th17-polarized cells induced more severe d

276 ribution is under circadian control and that AQP4 supports this rhythm.

277 Elimination of Aqp4 suppressed swelling-induced [Ca(2+)]i elevations bu

278 on optical imaging for measuring the size of AQP4 supramolecular clusters in paraffin sections of bra

279 Although multiple AQP4 T-cell epitopes have been identified in WT C57BL/6

280 uate how AQP4-specific T cells contribute to AQP4-targeted CNS autoimmunity (ATCA) and suggest that p

281 By contrast, expression of M1-AQP4 (AQP4-tetramers), which is unable to aggregate into OAP,

282 ween the actin cytoskeleton and AQP4-OAP and AQP4-tetramers.

283 tic serum IgG autoantibodies to aquaporin 4 (AQP4), the most abundant water-channel protein in the ce

284 Aquaporin-4 (AQP4), the primary water channel in glial cells of the m

285 of the water-permeable channel aquaporin-4 (AQP4) to astrocytic endfeet is dependent on interactions

286 idence for a gliogenetic basis that involves AQP4, underlying language-associated brain plasticity.

287 he expression, localization, and function of AQP4, using primary astrocytes as a model system.

288 al GM volume increase were modulated by this AQP4 variant, which was also associated with verbal lear

289 Expression of AQP4 was analyzed in postmortem frontal cortex of cognit

290 Expression of AQP4 was associated with advancing age among all individ

291 tting demonstrated that Muller cell-specific AQP4 was expressed at a higher level at the fovea than t

292 expression of structural proteins (GFAP and AQP4) was compromised.

293 ydrophilic peptide loops of the aquaporin-4 (AQP4) water channel are delivered to cytosolic and lumen

294 disorder mediated by pathogenic aquaporin-4 (AQP4) water channel autoantibodies (AQP4-IgG).

295 ow that the two isoforms of the aquaporin-4 (AQP4) water channel may determine the fate of gliomas.

296 Aquaporin-4 (AQP4) water channel-specific IgG distinguishes neuromyel

297 nism additionally suggests that aquaporin-4 (AQP4) water channels facilitate convective transport thr

298 noglobulin G (NMO-IgG) binds to aquaporin-4 (AQP4) water channels in the central nervous system leadi

299 f serum antibodies (Ab) against aquaporin-4 (AQP4), which unequivocally differentiate NMO from MS.

300 IgG-lacking Fc redistributes AQP4 within the plasma membrane and induces interleukin-