ライフサイエンスコーパス: GFAP

1 GFAP and other markers of enteric glial cells (eg, p75 a

2 GFAP expression was significantly reduced in the NAc cor

3 GFAP gene activation and protein induction appear to pla

4 GFAP is also subject to numerous post-translational modi

5 GFAP is the major astrocytic intermediate filament, and

6 GFAP mRNA expression is regulated by several nuclear-rec

7 GFAP peaked at 20 hours after injury and slowly declined

8 GFAP performed consistently in detecting MMTBI, CT lesio

9 GFAP yielded an AUC of 0.86 for differentiating between

10 GFAP(+)-Cre-dependent overexpression of xCT in vDG mimic

11 activity, however, was reduced in HIF-1alpha-GFAP Cre+ mice as indicated by a decrease in proinflamma

12 ic protein (GFAP) promoter (i.e., HIF-1alpha-GFAP Cre+ mice).

13 f necrotic cells was decreased in HIF-1alpha-GFAP Cre+ mice.

14 hese mice and control mice (i.e., HIF-1alpha-GFAP Cre- mice) were treated with a single dose of carbo

15 At 1week, GFAP was at the edge of detection, and in some experimen

16 Gfap(R236H/+) knock-in mice, which harbor a GFAP mutation homologous to one that causes AxD in human

17 To model human gliomagenesis, we used a GFAP-HRas(V12) mouse model crossed into the p53ER(TAM) b

18 Abnormal GFAP aggregation also occurs in giant axon neuropathy (G

19 These mutations result in abnormal GFAP accumulations that promote seizures, motor delays a

20 to trigger seizures, revealed that abnormal GFAP accumulation contributes to anomalous brain activit

21 ker NF200, nor glial fibrillary acidic acid (GFAP)-expressing supporting cell marker.

22 reveals that an AxD-causing mutation alters GFAP turnover kinetics in vivo and provides an essential

23 o), and glial activation (YKL-40, MCP-1, and GFAP).

24 trikingly similar redistribution of AQP4 and GFAP+ astrocytes transformed into clasmatodendrocytes.

25 s associated with increased VEGF, CD105, and GFAP and decreased ZO-1/occludin levels in the Cbs(+/-)

26 ositively correlated with levels of CD68 and GFAP transcripts in the striatum.

27 CA1, the density of GFAP-positive cells and GFAP expression rose during the first 2 weeks after birt

28 Apolipoprotein E and GFAP showed negative regional association with amyloid-b

29 AP-A7KO offspring from alpha7nAChR(flox) and GFAP-Cre crosses.

30 the brain correlated with increased Iba1 and GFAP staining, indicative of microglia and astrocyte rea

31 ls were similar in the brain of GFAP-IL6 and GFAP-IL6/sgp130 mice.

32 ur results demonstrate that blood UCH-L1 and GFAP are increased early after stroke and distinct bioma

33 Serum UCH-L1 and GFAP concentrations also strongly predicted poor outcome

34 Both UCH-L1 and GFAP concentrations were significantly greater in ICH pa

35 egulation of Oct4, SSEA, Neurofilament M and GFAP with significant decreases in both G2/M phase cells

36 Double labeling (with NeuN and GFAP) immunohistochemistry revealed that NFATc3 was expr

37 rast, the proportions of NeuN(+) neurons and GFAP(+) astrocytes that were immunopositive for activin

38 reasing profile over time in S100B, NSE, and GFAP.

39 +) (quiescent neural stem cells [qNSCs]) and GFAP(+)CD133(+)EGFR(+) (activated neural stem cells [aNS

40 hase and neurobiochemical changes (P-Tau and GFAP induction) in the subacute and chronic phase as wel

41 mical expression of beta-APP, ubiquitin, and GFAP in the retina and optic nerve.

42 find that filamentous proteins, vimentin and GFAP, are expressed by Muller glia, but have different p

43 (anti-glial fibrillary acidic protein [anti-GFAP]) and to investigate the blood-retinal barrier usin

44 In contrast to normal appearing GFAP+ astrocytes, clasmatodendrocytes were swollen and h

45 roblasts are remarkably unresponsive, as are GFAP(+) astrocytes found outside the SVZ.

46 ific precursor cell marker Nestin as well as GFAP and Sox2.

47 gradation of some but not all AxD-associated GFAP mutants.

48 EA4), neurons (Neurofilament M), astrocytes (GFAP) or cell cycle phase, the drug caused a 1.4-fold in

49 cascade through which aberrant astrocytosis/GFAP up-regulation potentiates neurotoxicity and contrib

50 rs in a transgenic mouse model of autoimmune GFAP meningoencephalitis.

51 ural autoantibody, which we discovered to be GFAP-specific, is disease spectrum restricted but not ra

52 AxD is a primary astrocyte disease because GFAP expression is specific to astrocytes in the central

53 e expression of reactive astrocyte biomarker GFAP within damaged tissue following TBI.

54 Both GFAP and UCH-L1 were detectible within 1 hour of injury.

55 ted by betaA3/A1-crystallin to modulate both GFAP and VEGF.

56 BrdU/beta-tubulin/HNA/DAPI, BrdU/GFAP/HNA/DAPI, Ngn1/DAPI, and BMP4/DAPI were measured by

57 ow that TSG-6 is expressed in the rat CNS by GFAP(+) and CD44(+) astrocytes, solely in the mature bra

58 ive overexpression of a single MMP driven by GFAP expressing cells in vivo.

59 FTIR and the glial distribution revealed by GFAP immunohistochemistry.

60 he gene network unique to ependymal CD133(+)/GFAP(-) quiescent cells were enriched for immune-respons

61 e uncovered molecular properties of CD133(+)/GFAP(-) ependymal (E) cells in the adult mouse forebrain

62 Immunohistochemical (anti-human vWF, CD45, GFAP, and Iba-1) and motor neuron histological analyses

63 lary acidic protein (GFAP)-expressing cells (GFAP(+) glial cells) are the predominant cell type in th

64 stainings using markers against glial cells (GFAP), endothelial cells (CD34) and macrophages (CD68) w

65 sion volume was observed between conditional GFAP/p38 MAPK knockout mice and littermates.

66 Fingolimod also decreased GFAP staining and the number of activated microglia.

67 e cells with processes resembling dendrites, GFAP-positive astrocytes, APC/CC1-positive oligodendrocy

68 e areas that showed the highest differential GFAP immunoreactivity between lean and obese animals inc

69 ed evidence permits to classify the dominant GFAP signatures in biological fluids.

70 enitor markers such as nestin, doublecortin, GFAP, neurofilament, and vimentin.

71 e uniformly composed of compacted elongated, GFAP-positive spindle cells (due to intermediate filamen

72 glial cells extended beyond that of enhanced GFAP staining and mapped more closely to the extent of (

73 However, exclusively GFAP differed in ICH compared with IS (p < 0.0001).

74 , particularly in the mucosa, do not express GFAP.

75 sion levels of glial intermediate filaments (GFAP, vimentin) and extracellular matrix components (lam

76 FAP-A7KO) to test whether alpha7nAChR(flox), GFAP-A7KO and appropriate littermate controls performed

77 I, 0.67-0.92) to 0.97 (95% CI, 0.93-1.00)for GFAP and 0.31 (95% CI, 0-0.63) to 0.77 (95% CI, 0.68-0.8

78 imetric and fluorescence based bioassays for GFAP was decreased by ~1000 times using the MAB techniqu

79 generally displayed high immunostaining for GFAP, S100beta, and CD44, but low immunostaining for glu

80 a neurosurgical intervention, the range for GFAP was 0.91 (95% CI, 0.79-1.00) to 1.00 (95% CI, 1.00-

81 These novel findings reveal unique roles for GFAP-positive glial and neuronal Panx1 and describe new

82 The overall bioassay time for GFAP and STX 1 was reduced from 4h using commercially av

83 cyte-derived neural stem cells isolated from GFAP-CreER-Notch1 conditional knockout (cKO) mice.

84 trocytes in hippocampal slices obtained from GFAP-A7KO offspring from alpha7nAChR(flox) and GFAP-Cre

85 e selective glial activation in tissues from GFAP::hM3Dq mice evoked electrogenic ion transport to an

86 Gliosis (GFAP) increased in all regions except the Nac but only P

87 Hippocampal gliosis (GFAP reactivity) was correlated with both abnormal behav

88 In CCI-vehicle, sham and CCI-SR49059 groups, GFAP was 1.58+/-0.04, 0.47+/-0.02, and 0.81+/-0.03, resp

89 Higher GFAP levels were associated with stroke severity and his

90 However, GFAP-IL6/sgp130 mice had decreased pY(705)-STAT3 in the

91 xpression of synapsin-Cre or inducible human GFAP-CreERT2.

92 d B-FABP promoters in NFI-hypophosphorylated GFAP/B-FABP+ve MG cells.

93 In GFAP-specific CD8 TCR-transgenic (BG1) mice, tissue resi

94 However, Snf5 ablation in GFAP-positive cells caused a neurodegenerative phenotype

95 aracteristic of GFAP-IL6 mice were absent in GFAP-IL6/sgp130 mice.

96 By contrast, gliomas arising in GFAP-HRas(V12);p53(KI/KI) mice develop in the absence of

97 Calcineurin in GFAP/B-FABP+ve MG cells localizes to the nucleus.

98 +AA+GCV, there was a significant decrease in GFAP and desmin-positive cells, compared to WT mice ( ap

99 The TSPO-/- mouse showed a decrease in GFAP expression, correlating with a decrease in astrogli

100 ve gliosis, as demonstrated by a decrease in GFAP immunolabeling, and suppressed the activation of ma

101 Panx1 deletion in GFAP-positive glia cells prevented hypersensitivity comp

102 disease tissue, where ASPP2 was detected in GFAP-expressing reactive astrocytes that coexpress STAT1

103 Surprisingly, gliomas that develop in GFAP-HRas(V12);p53(+/KI) mice abrogate the p53 pathway b

104 beta-actin-GFP drove transgene expression in GFAP(+) astrocytes.

105 ppocampal neurogenesis which was impaired in GFAP-IL6 mice was rescued in young GFAP-IL6 mice with ce

106 fibrogenic chemokine CCL3 and an increase in GFAP(+) fibrogenic cells.

107 r structures as well as two-fold increase in GFAP-positive fibers as compared with those in controls.

108 with genetically encoded Ca(2+) indicator in GFAP-positive glia or in neurons, both cell populations

109 conditional deletion of p38alpha (MAPK14) in GFAP+ astrocytes.

110 rocytes, caused by heterozygous mutations in GFAP, which encodes the major astrocyte intermediate fil

111 Targeted deletion of Panx1 in GFAP-positive glia or in neurons revealed distinct effec

112 ice or activating glial calcium responses in GFAP::hM3Dq mice, and tested the effects on colonic barr

113 Likewise, in vivo studies in GFAP-Tat tg mice showed increased autophagosome accumula

114 This was confirmed in vivo in GFAP-IR KO mice by using positron emission tomography an

115 nificantly increased in regions of increased GFAP immunoreactivity and OX-42 colocalization, meaning

116 NA targeting the hypothalamus also increases GFAP mRNA within the female hypothalamus on PN2, suggest

117 tional knock-out of beta1-integrin increases GFAP expression and astrocytic differentiation by cultur

118 CASP2 treatment also significantly increases GFAP+ glial activation, increases the expression of CNTF

119 We have shown that that Tat induces GFAP expression in astrocytes and that GFAP activation i

120 In contrast, a viral trigger induces GFAP-specific CD8 T effector cells to exclusively target

121 tion of EZC progeny that differentiated into GFAP+ astrocytes, and diminished functional recovery.

122 We therefore sought to directly investigate GFAP turnover in a mouse model of AxD that is heterozygo

123 Here, we prospectively isolate GFAP(+)CD133(+) (quiescent neural stem cells [qNSCs]) an

124 dose at 1h after injury reduces the NO, LPO, GFAP and MPO level at injury site by increasing the expr

125 95 (now known as DLG4), the astrocyte marker GFAP, other molecules related to amyloid-beta metabolism

126 , proper expression of the astrocytic marker GFAP and corticogenesis.

127 ncreased expression of the astrocytic marker GFAP in the cortex of 7-day old pups.

128 d up-regulating the glial maturation marker, GFAP.

129 brillary acidic protein-luc transgenic mice (GFAP-luc mice).

130 cible transgenic GFAP-CreER-Notch1-cKO mice, GFAP-CreER-ETB(R)-cKO mice exhibited a defect in reactiv

131 y, we subjected C3a receptor-deficient mice, GFAP-C3a transgenic mice expressing biologically active

132 MKO(GFAP) mice exhibit moderately increased 2-AG and reduced

133 etion of MGL specifically in astrocytes (MKO(GFAP)).

134 Importantly, MKO(GFAP) mice exhibit reduced brain prostaglandin E2 and pr

135 nor accumulation of 2-AG in the brain of MKO(GFAP) mice does not cause cannabinoid receptor desensiti

136 ine kinase gene (HSV-Tk) driven by the mouse GFAP promoter were used to render proliferating HSCs sus

137 reased, abnormal levels of astrocytic mutant GFAP in the development and progression of the epileptic

138 The mechanisms by which mutant GFAP leads to these pleiotropic effects are unknown.

139 production of new neurons in socially naive GFAP-thymidine kinase rats showed that loss of 6-week-ol

140 tification of SMI312(+) dystrophic neurites, GFAP(+) reactive astrocytes, and IBA1(+) and CD68(+) act

141 Some cortical NeuN(+) neurons, GFAP(+) glia limitans astrocytes, Iba-1(+) microglia and

142 Neither alpha7nAChR(flox) nor GFAP-A7KO exhibited significant differences from litterm

143 endent of parasite burden and the ability of GFAP(+) astrocytes to physically encircle parasites.

144 ng or reversing pathological accumulation of GFAP as a potential therapeutic strategy for AxD and rel

145 s characterized by excessive accumulation of GFAP, known as Rosenthal fibers, within astrocytes.

146 e of the disease is aberrant accumulation of GFAP.

147 t preventing or reducing the accumulation of GFAP.

148 e accumulation of extremely large amounts of GFAP causes many molecular changes in astrocytes, includ

149 es, glial seal formation, and attenuation of GFAP expression after complete photoreceptor loss.

150 L-6 mRNA levels were similar in the brain of GFAP-IL6 and GFAP-IL6/sgp130 mice.

151 changes in the cerebellum characteristic of GFAP-IL6 mice were absent in GFAP-IL6/sgp130 mice.

152 tion of proteasome reversed the clearance of GFAP in cells achieved by overexpressing gigaxonin.

153 Although the clustering of GFAP immunopositive astrocytes around amyloid-beta plaqu

154 transmission regulating GABAergic control of GFAP(+) cells during early postnatal development.

155 igaxonin levels influence the degradation of GFAP in primary astrocytes and in cell lines that expres

156 gigaxonin is involved in the degradation of GFAP.

157 In CA1, the density of GFAP-positive cells and GFAP expression rose during the

158 ed the iCrystal system) for the detection of GFAP from mice with brain injuries and STX 1 from a city

159 ioassay platforms for the rapid detection of GFAP in buffer based on colorimetric and fluorescence re

160 ular, these data suggest that elimination of GFAP might be possible and occurs more quickly than prev

161 The conjoint increased expression of GFAP and MMP-9 and a purinergic ATP (P2) receptor antago

162 T3 and Cryba1 could potentiate expression of GFAP and secretion of VEGF, both of which are essential

163 Expression of GFAP has been reported in some of the tumor types identi

164 V-TK) mice and epithelial-cell expression of GFAP.

165 ssion or GFAP expression led to formation of GFAP aggregates and induction of unfolded protein respon

166 r elucidating the regulation and function of GFAP can contribute to our understanding of MeCP2 functi

167 f Muller cells processes, hyperexpression of GFAP, and preservation of normal electrophysiology follo

168 nimals.Increased retinal immunoreactivity of GFAP, RAGE, TNF-alpha, VEGF and 5-LO was seen in diabeti

169 CI-SR49059 groups, fluorescence intensity of GFAP was 349+/-38, 56+/-5, and 244+/-30, respectively, V

170 ocytes towards injury and the involvement of GFAP in the progression of AxD.

171 V-Gfa2-VIVIT had no effects on the levels of GFAP and Iba1, suggesting that synaptic benefits of VIVI

172 We observed higher serum levels of GFAP and UCH-L1 in brain-injured children compared with

173 In obese animals high levels of GFAP immunoreactivity were often associated with the mic

174 e current literature on body fluid levels of GFAP in human disease is summarised and illustrated by d

175 als revealed that, in vivo, the half-life of GFAP in mutant mice (15.4 +/- 0.5 days) was much shorter

176 r damage, we assessed the co-localization of GFAP and AQP4 immunoreactivities in post-mortem brains f

177 resence of GABArho in the plasma membrane of GFAP(+) cells.

178 In situ monitoring of GFAP, Ki67, caspase-3, Beclin-1, and LC-3 in the tumor s

179 TSG-6(-/-) mice present a reduced number of GFAP(+) astrocytes when compared with the littermate TSG

180 Overexpression of GFAP is an indicator of astrogliosis/neuroinflammation i

181 reatment for 1 h increases the percentage of GFAP-positive astrocytes that show enhanced Px1 HC-media

182 We also confirmed the potential of GFAP as a tool for early rule-in of ICH, while UCH-L1 wa

183 2-GLT1 resulted in transduction primarily of GFAP(+) astrocytes that persisted for >/=6 weeks postinj

184 perinuclear space and along the processes of GFAP(+) cells.

185 But, neither quantification of GFAP-positive cells nor the Western blot analysis indica

186 (STAT3) is involved in the co-regulation of GFAP and VEGF.

187 9 suppressed injury-induced up regulation of GFAP, V1A and AQP4, blunting edematous changes.

188 Our results point to a role of GFAP and UCH-L1 as candidate biomarkers for pediatric TB

189 In addition to the role of GFAP as a diagnostic biomarker for chronic disease, ther

190 Our understanding of the role of GFAP(+) glial cells and their signalling systems in vivo

191 indings reveal an unexpectedly broad role of GFAP(+) glial cells in modulating complex physiology and

192 at alpha7 nAChR binding sites were absent on GFAP-positive astrocytes in hippocampal slices obtained

193 this study, we showed that Tat expression or GFAP expression led to formation of GFAP aggregates and

194 , we demonstrated that inhibition of Tat- or GFAP-induced UPR/ER stress by the chemical chaperone 4-p

195 sence of glial- and neuronal cell phenotype (GFAP and Nestin-1 positivity, respectively) in the iERMs

196 Positive GFAP expression was detected in the control positive gro

197 ng glial fibrillary acidic protein-positive (GFAP(+)) reactive astrocytes after stroke.

198 idic fibrillary protein (GFAP)-Cre promoter (GFAP-A7KO) to test whether alpha7nAChR(flox), GFAP-A7KO

199 oding the intermediate filament (IF) protein GFAP.

200 sitive and/or glial fibrillary acid protein (GFAP)-positive progenitor cells of the developing centra

201 yte marker, glial fibrillary acidic protein (GFAP) and a protease, matrix metallopeptidase 9 (MMP-9).

202 staining of glial fibrillary acidic protein (GFAP) and CD45 for the detection of reactive astrocytes

203 lial marker glial fibrillary acidic protein (GFAP) and in Slit2 at the glial wedge and indusium grise

204 etection of Glial Fibrillary Acidic Protein (GFAP) and Shiga like toxin (STX 1).

205 stained for glial fibrillary acidic protein (GFAP) and Toll-like receptor 2 (TLR2).

206 Glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase L1 (UCH-L1) hav

207 trations of Glial Fibrillary Acidic Protein (GFAP) and Ubiquitin C-Terminal Hydrolase-L1 (UCH-L1) in

208 ssible with glial fibrillary acidic protein (GFAP) antibodies.

209 the role of glial fibrillary acidic protein (GFAP) as a biomarker for astroglial pathology in neurolo

210 o increased glial fibrillary acidic protein (GFAP) expression and aggregation and activation of unfol

211 e increased glial fibrillary acidic protein (GFAP) expression in the brain.

212 s including glial fibrillary acidic protein (GFAP) expression, surface area, volume, and colocalizati

213 h increased glial fibrillary acidic protein (GFAP) expression.

214 (VEGF) and glial fibrillary acidic protein (GFAP) expressions were detected by immunohistochemical s

215 d with anti-glial fibrillary acidic protein (GFAP) immunohistochemistry to provide a comparison betwe

216 cells, the glial fibrillary acidic protein (GFAP) immunoreactivity, and the ultrastructure of the sy

217 Glial fibrillary acidic protein (GFAP) is an intermediate filament (IF) III protein uniqu

218 Glial fibrillary acidic protein (GFAP) is the major intermediate filament of mature astro

219 te filament glial fibrillary acidic protein (GFAP) lead to the rare and fatal disorder, Alexander dis

220 autoimmune glial fibrillary acidic protein (GFAP) meningoencephalomyelitis from disorders commonly c

221 rrespond to glial fibrillary acidic protein (GFAP) mRNA (AS-gfap or S-gfap, respectively) expression.

222 aining with glial fibrillary acidic protein (GFAP) or S100beta.

223 trol of the glial fibrillary acidic protein (GFAP) promoter (i.e., HIF-1alpha-GFAP Cre+ mice).

224 S: When the glial fibrillary acidic protein (GFAP) promoter is used to express cellular toxins that e

225 cell marker glial fibrillary acidic protein (GFAP) to study the incidence and location of clasmatoden

226 f OX-42 and glial fibrillary acidic protein (GFAP) was performed to identify activated microglial cel

227 n (SOM) and glial fibrillary acidic protein (GFAP), a marker for astrogliosis during neurodegeneratio

228 reactive to glial fibrillary acidic protein (GFAP), a protein expressed in astrocytes, can avoid tole

229 e 1 (Iba1), glial fibrillary acidic protein (GFAP), and the fractalkine receptor CX3CR1 in DRGs.

230 CD34, p53, glial fibrillary acidic protein (GFAP), CD163, and Ki67 (cell replication) were employed;

231 imentin and glial fibrillary acidic protein (GFAP), excluding the possibility of an ependymal nature.

232 (NSE), and glial fibrillary acidic protein (GFAP), in addition to multiple inflammatory markers.

233 emistry for glial fibrillary acidic protein (GFAP), rhodopsin, S-cone opsin, and M/L-cone opsin were

234 showed that glial fibrillary acidic protein (GFAP), tyrosine receptor kinase B (TrkB) and substance P

235 100beta and glial fibrillary acidic protein (GFAP), were used as indicator for neural differentiation

236 gous Tyr in glial fibrillary acidic protein (GFAP), which is mutated in Alexander disease (Y242D).

237 biomarker, glial fibrillary acidic protein (GFAP)-breakdown product (GBDPs) in injured cortex were a

238 Glial fibrillary acidic protein (GFAP)-expressing cells (GFAP(+) glial cells) are the pre

239 rs (IRs) in glial fibrillary acidic protein (GFAP)-expressing cells affects hypothalamic astrocyte mo

240 sorder with glial fibrillary acidic protein (GFAP)-IgG as biomarker was recently characterized.

241 tiation into glial fibrillar acidic protein (GFAP)-immunoreactive cells over neurons, while overexpre

242 ctivity for glial fibrillary acidic protein (GFAP).

243 ne encoding glial fibrillary acidic protein (GFAP).

244 cific gene, glial fibrillary acidic protein (GFAP).

245 nt protein, glial fibrillary acidic protein (GFAP).

246 te filament glial fibrillary acidic protein (GFAP).

247 iosis [anti-glial fibrillary acidic protein (GFAP)], pericytes (anti-neural/glial antigen 2), blood-r

248 ositive for glial fibrillary acidic protein (GFAP+) expressed gastrin de novo through a mechanism tha

249 L1) and glial fibrillary astrocytic protein (GFAP) in acute stroke patients and healthy controls and

250 iven by the glial acidic fibrillary protein (GFAP)-Cre promoter (GFAP-A7KO) to test whether alpha7nAC

251 ncrease in glial fibrillary acidic protein+ (GFAP+), but not in NG2+, cell proliferation in vitro.

252 Four of the up-regulated proteins (GFAP, high affinity glutamate transporter (EAAT-2), apo-

253 the mRNA expression of structural proteins (GFAP and AQP4) was compromised.

254 Rare GFAP-IgG positivity was encountered in serum controls by

255 continuous borders and significantly reduced GFAP density.

256 CCI significantly up-regulated GFAP, V1aR and AQP4 protein levels and SR49059 suppresse

257 ocytosis was astrocyte-specific and required GFAP expression and was mediated by ER stress.

258 alization of aquaporin 4 (AQP4) in retracted GFAP+ astrocytes with disrupted end-feet juxtaposed to m

259 ifically modulating the expression of S100B, GFAP, inducible nitric oxide synthase, and thrombospondi

260 ted TBI-induced increases in serum S100beta, GFAP, and neuron specific enolase.

261 ) confirmation of IgG reactive with specific GFAP isoforms (alpha, varepsilon, or kappa) by cell-base

262 c brain and spinal cord injuries and stroke, GFAP and its breakdown products are rapidly released int

263 s of the GFAP promoter region and suppresses GFAP expression in vitro.

264 essed the stem cell markers Slc1a3-CreER(T), GFAP-CreER(T2), Sox2(CreERT2), and Gli1(CreERT2) and wer

265 igaxonin as an important factor that targets GFAP for degradation through the proteasome pathway.

266 Bigenic mice (termed GFAP-IL6/sgp130 mice) were generated with CNS-restricted

267 ice, although at a later age (9 months) than GFAP and Abeta.

268 duces GFAP expression in astrocytes and that GFAP activation is indispensable for astrocyte-mediated

269 Here we demonstrate that GFAP(+) cells of the granular layer of cerebellum expres

270 In addition, we demonstrated that GFAP up-regulation and aggregation in astrocytes were ne

271 Here, we show that GFAP::Cre;Erbb3(F/F) mice, which lack Erbb3 in both radi

272 The GFAP immunoreactivity of astrocytes, but not the MHC2 im

273 The GFAP signal, revealed by bioluminescent imaging in the l

274 fluorescent protein (Lck-GFP) driven by the GFAP promoter, coupled with synapsin I immunohistochemis

275 h is caused by heterozygous mutations in the GFAP gene, which is the gene that encodes the major astr

276 eduction of astrogliosis was observed in the GFAP/p38 knockout mice compared with the littermates.

277 precipitation, we show that NFI occupies the GFAP and B-FABP promoters in NFI-hypophosphorylated GFAP

278 MeCP2 binds to methylated regions of the GFAP promoter region and suppresses GFAP expression in v

279 ckade of trans-signaling in the brain of the GFAP-IL6 mice significantly attenuated Serpina3n but not

280 evels on gliomagenesis in the context of the GFAP-V12Ha-ras-IRESLacZ (Ras*) model.

281 Third, in contrast to the GFAP-Cre strain, Nf1 gene inactivation in NG2+ cells is

282 Second, similar to the GFAP-Cre transgenic strain that drives Nf1 optic gliomag

283 astrocytes and causes neurotoxicity through GFAP activation and ER stress induction in astrocytes an

284 te filament, and in AxD patient brain tissue GFAP is a major component of RFs.

285 In addition, gigaxonin directly bound to GFAP, and inhibition of proteasome reversed the clearanc

286 Total GFAP+ cells in both the frontal and temporal white matte

287 icated that the in vitro half-lives of total GFAP in astrocytes from wild-type and mutant mice were s

288 Similar to inducible transgenic GFAP-CreER-Notch1-cKO mice, GFAP-CreER-ETB(R)-cKO mice e

289 on of adult neurogenesis in naive transgenic GFAP-thymidine kinase rats resulted in social behavior s

290 ansgenic mice overexpressing human wild-type GFAP.

291 Ablation of Nsdhl in radial glia using GFAP-cre resulted in live-born, normal appearing affecte

292 Levels of VEGF, GFAP, ZO-1, and occludin were determined by immunoblotti

293 Over the course of 1 week, GFAP demonstrated a diagnostic range of areas under the

294 st-translational modifications (PTMs), while GFAP mutations result in protein deposits known as Rosen

295 howed a very strong inverse correlation with GFAP levels and ELISA measurements of Abeta, but not wit

296 ministration and extinction were paired with GFAP Westerns, immunohistochemistry, and fluorescent ima

297 Here, 102 patients with GFAP-IgG positivity are described.

298 Similar to K8, Y242D GFAP exhibited highly irregular filament organization an

299 ut, Yap(nestin) conditional knockout and Yap(GFAP) conditional knockout mice displayed fewer neocorti

300 paired in GFAP-IL6 mice was rescued in young GFAP-IL6 mice with cerebral sgp130 production.