ライフサイエンスコーパス: AQP4

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

2 mented by vasopressin-regulated aquaporin-4 (AQP4).

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

4 ytes, TRPV4 activation became independent of AQP4.

5 distinct physiological roles for M1- and M23-AQP4.

6 comparison to transfectants expressing only AQP4.

7 ers specific functional roles to M1- and M23-AQP4.

8 nnel in Xenopus laevis oocytes together with AQP4.

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

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

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

12 -1.1 yrs) for AQP4-Ab positive vs 2.4 yrs in AQP4-Ab negative cases (95% CI 1.1-3.6 yrs).

13 n in >/= 1 eye (0/8 AQP4-Ab negative), and 3 AQP4-Ab negative cases were wheelchair-dependent.

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 sual acuity < 6/60 Snellen in >/= 1 eye (0/8 AQP4-Ab negative), and 3 AQP4-Ab negative cases were whe

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

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

19 0.9% and with a specificity of 87.1% against AQP4-ab NMOSD, 95.2% against MOG-ab NMOSD and 87.5% in t

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

21 In AQP4-Ab positive cases, 10/12 had visual acuity < 6/60 S

22 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

23 th early recurrence and visual impairment in AQP4-Ab positivity and physical disability in AP4-Ab neg

24 rospinal fluid of patients with NMO, induces AQP4-ab production by plasmablasts and represents a nove

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

26 Early AQP4-Ab testing may allow prompt immunomodulatory treatm

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

28 l cord and brain magnetic resonance imaging, AQP4-ab titers, pain levels (numerical rating scale), an

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

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

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

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

33 Patients with AQP4-Ab-negative NMO/NMOSD should be tested for MOG-Abs.

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

35 a trend toward older age at disease onset in AQP4-Ab-positive patients (44.9 vs 32.3 years; P = .05).

36 Twenty AQP4-Ab-positive patients and 9 MOG-Ab-positive patients

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

38 Ninety percent of AQP4-Ab-positive patients but only 44% MOG-Ab-positive p

39 A higher proportion of AQP4-Ab-positive patients relapsed (40% vs 0%; P = .03)

40 112 patients with NMOSD (31 AQP4-ab-positive, 21 MOG-ab-positive, 16 ab-negative) or

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

42 atures of both NMO and MS, test negative for AQP4-Abs and may be difficult to definitively diagnose.

43 were used to test patient serum samples for AQP4-Abs and MOG-Abs.

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

45 rvice and who tested positive for MOG-Abs or AQP4-Abs were included in the study.

46 der have autoantibodies against aquaporin-4 (AQP4-Abs), but recently, myelin-oligodendrocyte glycopro

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

48 differences when compared with patients with AQP4-Abs.

49 re differences when compared with those with AQP4-Abs.

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

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

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

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

54 effect caused by heterodimerization between AQP4 and AQP4-Delta4, which was detected in coimmunoprec

55 The sarcolemma exhibited loss of AQP4 and deposition of IgG and complement activation pro

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

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

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

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

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

61 of the astrocytic water channel aquaporin-4 (AQP4) and changes in glymphatic pathway function was eva

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

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

64 of astrocytic laminin decreases aquaporin-4 (AQP4) and tight junction protein expression.

65 ination of antibodies to NMDAR, aquaporin-4 (AQP4), and myelin oligodendrocyte glycoprotein (MOG) was

66 essed transcription of genes encoding Trpv4, Aqp4, and the Kir4.1 subunit of inwardly rectifying pota

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

68 Patients with AQP4 antibodies (median visual score, 3.5 [range, 1-9])

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

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

71 isolated ON, and the patient with concurrent AQP4 antibodies had conversion to neuromyelitis optica.

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

73 50 anti-NMDAR and 1 of 56 NMO patients, and AQP4 antibodies in 48 of 56 NMO and 1 of 50 anti-NMDAR p

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

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

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

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

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

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

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

81 from multiple sclerosis but overlapped with AQP4 antibody disease.

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

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

84 Aquaporin 4 (AQP4) appeared distributed all over the cell bodies and

85 an alternatively spliced transcript of human AQP4, AQP4-Delta4, that lacks exon 4.

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

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

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

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

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

91 trate that large AQP4 clusters are formed in AQP4(-/-) astrocytes transfected with only M23-AQP4, but

92 atients were retested with recombinant human AQP4-based assays, including enzyme-linked immunosorbent

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

94 23-AQP4, but not in those expressing only M1-AQP4, both in vitro and in vivo.

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 P4(-/-) astrocytes transfected with only M23-AQP4, but not in those expressing only M1-AQP4, both in

98 Thus, the regulation of AQP4 by GABA(A)Rs is involved in controlling activation

99 tivity reflects targeting of skeletal muscle AQP4 by pathogenic IgG.

100 of loop C conformation to the recognition of AQP4 by pathogenic NMO Abs.

101 e with targeting of sarcolemmal aquaporin-4 (AQP4) by complement-activating IgG implies involvement o

102 ace expression and therefore the activity of AQP4 can be physiologically modulated.

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

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

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

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

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

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

109 ution optical imaging methodology to measure AQP4 cluster size in antibody-stained paraffin sections

110 eurological diseases and we demonstrate that AQP4 clustering was preserved in a postmortem human cort

111 thodology was used to demonstrate that large AQP4 clusters are formed in AQP4(-/-) astrocytes transfe

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

113 cromolecular interactions of small and large AQP4 clusters results in distinct physiological roles fo

114 urprisingly, the subcellular distribution of AQP4 clusters was different between gray and white matte

115 ng size-dependent subcellular segregation of AQP4 clusters.

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

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

118 d in </=0.1% of individuals (anti-AMPAR-1/2, AQP4, CV2, Tr/DNER, DPPX-IF1, GABAR-B1/B2, GAD67, GLRA1b

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

120 s suggest that the neuroprotective effect of AQP4 deletion in global cerebral ischemia involves reduc

121 In transfected cells AQP4-Delta4 is mainly retained in the endoplasmic reticu

122 When AQP4-Delta4 is transfected into cells stably expressing

123 The expression of AQP4-Delta4 may represent a new regulatory mechanism thr

124 In skeletal muscles, AQP4-Delta4 mRNA expression inversely correlates with th

125 ernatively spliced transcript of human AQP4, AQP4-Delta4, that lacks exon 4.

126 aused by heterodimerization between AQP4 and AQP4-Delta4, which was detected in coimmunoprecipitation

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

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

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

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

131 Functional synergy between TRPV4 and AQP4 during cell swelling was confirmed in the heterolog

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

133 e to diffusional sieving of small, mobile M1-AQP4-enriched arrays into lamellipodia and preferential

134 a and preferential interaction of large, M23-AQP4-enriched arrays with the extracellular matrix.

135 tor repertoires for recognition of these two AQP4 epitopes.

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

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

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

139 GABA(A)R signaling promotes AQP4 expression by decreasing serine phosphorylation ass

140 The modulation of AQP4 expression by GABA(A)R signaling is key to its effe

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

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

143 AQP4 expression was increased in white matter around lat

144 AQP4 expression was significantly increased 24 hours aft

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

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

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

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

149 Co-expressed M1- and M23-AQP4 formed aggregates of variable size that segregated

150 In contrast, M23-AQP4 formed large arrays that did not diffuse rapidly en

151 The water channel aquaporin-4 (AQP4) forms supramolecular clusters whose size is determ

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

153 y modulates volume regulation, swelling, and Aqp4 gene expression.

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

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

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

157 Patients with STM who were seronegative for AQP4-IgG among an Olmsted County population-based cohort

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

159 4 allowed us to infer the size of individual AQP4-IgG binding events.

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

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

162 ransfected cell-based assay (CBA), we tested AQP4-IgG in a northern California population representat

163 Sensitive serological evaluation for AQP4-IgG in this large population-representative cohort

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

165 th negative IIF results were reclassified as AQP4-IgG positive, yielding an overall AQP4-IgG seroposi

166 Twenty-five patients who were AQP4-IgG seropositive with an initial STM represented 14

167 ed as AQP4-IgG positive, yielding an overall AQP4-IgG seropositivity rate of 89%.

168 Recurrent hyperCKemia accompanying AQP4-IgG seropositivity reflects targeting of skeletal m

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

170 tense lesion less than 3 vertebral segments, AQP4-IgG seropositivity, and a final diagnosis of NMO or

171 lapsing optic neuritis, transverse myelitis, AQP4-IgG seropositivity, and recurrent myalgias with hyp

172 AQP4-IgG serostatus, clinical characteristics, and Expan

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

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

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

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

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

178 e relapse rate in both AQP4-IgG-positive and AQP4-IgG-negative patients with rLETM.

179 The female to male ratio was 2:3 for AQP4-IgG-negative rLETM and 5:1 for AQP4-IgG-positive pa

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

181 ant therapy reduced the relapse rate in both AQP4-IgG-positive and AQP4-IgG-negative patients with rL

182 Control patients included 140 AQP4-IgG-positive patients with NMO, of whom a subgroup

183 s similar to the median disease duration for AQP4-IgG-positive patients with rLETM (59 months).

184 The median number of attacks was 3 for AQP4-IgG-positive patients with rLETM (range, 2-22), and

185 From Kaplan-Meier analyses, 36% of AQP4-IgG-positive patients with rLETM are anticipated to

186 The AQP4-IgG-positive patients with rLETM or rLETM-onset NMO

187 2:3 for AQP4-IgG-negative rLETM and 5:1 for AQP4-IgG-positive patients.

188 Evolution to NMO can be anticipated in AQP4-IgG-positive patients.

189 In AQP4-IgG-positive STM cases, subsequent myelitis episode

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

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

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

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

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

195 concurrent with MOG in 3 and concurrent with AQP4 in 1).

196 atients (45%), including MOG in 10 patients, AQP4 in 6 patients, and GlyR in 7 patients (concurrent w

197 e was strong neuroprotection in mice lacking AQP4 in a model of global cerebral ischemia produced by

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

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

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

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

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

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

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

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

206 Therefore, TRPV4-AQP4 interactions constitute a molecular system that fin

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

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

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

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

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

212 the expression and water channel activity of AQP4 is likely to originate from a dominant-negative eff

213 The astrocyte water channel aquaporin-4 (AQP4) is expressed as heterotetramers of M1 and M23 isof

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

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

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

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

218 ze is determined by the ratio of M1- and M23-AQP4 isoforms.

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

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

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

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

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

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

225 Perivascular AQP4 localization was significantly associated with AD s

226 of the CD44+ astrocytes, while, in contrast, AQP4 localized to perivascular end feet in the CD44- pro

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

228 formational epitopes involving extracellular AQP4 loops A, C, and E.

229 Using an aquaporin-4 (AQP4) M1-isoform-specific enzyme-linked immunosorbent as

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

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

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

233 We conclude that AQP4-mediated water fluxes promote the activation of the

234 ation were much reduced in the AQP4(-/-) vs. AQP4(+/+) mice after carotid artery occlusion, as were b

235 e were greatly improved in the AQP4(-/-) vs. AQP4(+/+) mice after occlusion, with large and robust di

236 However, retinas from Trpv4(-/-) and Aqp4(-/-) mice exhibited suppressed transcription of gen

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 The entity of autoimmune AQP4 myopathy extends the neuromyelitis optica spectrum

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

243 recurrent isolated ON had antibodies to MOG, AQP4, or GlyR.

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

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

246 te water permeability secondary to defective AQP4 plasma membrane targeting.

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

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

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

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

251 terioles and widespread loss of perivascular AQP4 polarization along the penetrating arteries accompa

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

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

254 ica (NMO) spectrum disorder (5 cases, 4 anti-AQP4 positive) or brainstem or multifocal demyelinating

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

256 Here we review distinct features of AQP4-positive NMO and MS, which might then be useful in

257 nd M23 isoforms in which the presence of M23-AQP4 promotes formation of large macromolecular aggregat

258 ssion inversely correlates with the level of AQP4 protein and is physiologically associated with diff

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

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

261 d we evaluated the effects on binding of NMO AQP4-reactive rAbs by quantitative immunofluorescence.

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

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

264 r (V1aR) inhibition would suppress astrocyte AQP4, reduce astrocytic edema, and thereby diminish TBI-

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

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

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

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

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

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

271 Changes in AQP4 subcellular distribution are associated with severa

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

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

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

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

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

277 cted into cells stably expressing functional AQP4, the surface expression of the full-length protein

278 Here we hypothesize a pivotal role for AQP4 transmembrane regions (TMs) in epitope assembly.

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

280 racellular loops of the M23 isoform of human AQP4 using both serial and single point mutations, and w

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

282 water accumulation were much reduced in the AQP4(-/-) vs. AQP4(+/+) mice after carotid artery occlus

283 logical outcome were greatly improved in the AQP4(-/-) vs. AQP4(+/+) mice after occlusion, with large

284 00+/-0.06, 0.45+/-0.05, and 0.46+/-0.09; and AQP4 was 2.03+/-0.34, 0.49+/-0.04, and 0.92+/-0.22.

285 was 601+/-71, 117.8+/-14, and 390+/-76, and AQP4 was 818+/-117, 158+/-5, and 458+/-55 (n=3/group).

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

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

288 Individually expressed M1-AQP4 was freely mobile in the plasma membrane and could

289 man cortical brain tissue specimen, but that AQP4 was not substantially clustered in a human glioblas

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

291 NA expression of water channel, aquaporin 4 (AQP4) was increased after Dp71 deletion.

292 AQP4 water transport inhibition may improve survival and

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

294 ntial isoform 4 (TRPV4) and the aquaporin 4 (AQP4) water channel in retinal Muller cells.

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

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

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

298 inal-truncated human MOG and full-length M23-AQP4 were used to test patient serum samples for AQP4-Ab

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-