ライフサイエンスコーパス: GFAP

1 GFAP and GS concentrations differed significantly across

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

3 GFAP concentration was significantly positively correlat

4 GFAP expression does not increase with age in chimpanzee

5 GFAP expression was significantly reduced in the NAc cor

6 GFAP peaked at 20 hours after injury and slowly declined

7 GFAP performed consistently in detecting MMTBI, CT lesio

8 GFAP successful detection is demonstrated in a clean-buf

9 GFAP yielded an AUC of 0.86 for differentiating between

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

11 GFAP, Iba1, alphaII-spectrin, and SBDP remained unchange

12 GFAP-ARO-KO mice were viable and fertile, with normal gr

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

14 t drastically shifted differentiation to 80% GFAP cells (p < 0.05).

15 AAV5-GFAP-Cre-GFP particles were infused into the SN of 8-wee

16 Infusion of AAV5-GFAP-Cre-GFP vectors into the SN resulted in region-spec

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

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

19 tion of astrocyte and microglial activation (GFAP and CD68) and HMGB1 at 2 hr, 6 hr, 24 hr, 3 days, a

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

21 signatures and ensuing release of Iba-1 and GFAP into the circulation.

22 n diffuse injury, monitoring serum Iba-1 and GFAP levels can provide clinically relevant insight into

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

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

25 istry was performed against amyloid-beta and GFAP.

26 f-L > 25.5pg/ml had 110% faster decline, and GFAP > 232pg/ml had 130% faster decline compared to thos

27 that n-3 PUFAs increased GFAP expression and GFAP positive cell formation.

28 We hypothesise that elevated GS and GFAP levels could identify those double-Ab-seronegative

29 Cerebrospinal fluid concentrations of GS and GFAP were measured by ELISA in patients with NMOSD (n=39

30 GS and GFAP were significantly correlated, particularly in pati

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

32 mparison to immunofluorescence with Iba1 and GFAP.

33 e notable: t-tau 8 to 16 years, and Nf-L and GFAP 4 to 8 years prior to clinical AD.

34 rd ventricular volume, and baseline Nf-L and GFAP were associated with faster decline in cortical thi

35 Serum t-tau, Nf-L, and GFAP predict the development of sporadic AD and cognitiv

36 for serum concentrations of t-tau, Nf-L, and GFAP were measured in a population sample of 1,327 parti

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

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

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

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

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

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

43 TDF administered to wild-type (wt) and GFAP-gp120 transgenic (tg) mice caused peripheral neurop

44 Tau (pTau), amyloid precursor protein (APP), GFAP, Iba1, alphaII-spectrin, and spectrin breakdown pro

45 Immunohistochemistry for pTau, APP, GFAP, and Iba1 was performed.

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

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

48 Interestingly, BMP4 increased astrocytic GFAP expression, and BMP4-treated astrocytes failed to p

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 europathological analyses of BACHD and BACHD/GFAP-CreERT2-tam mice.

52 and electrophysiological phenotypes in BACHD/GFAP-CreERT2-tam mice compared to BACHD mice.

53 Behavioral analyses of BACHD/GFAP-CreERT2-tam mice demonstrate significant improvemen

54 protein in the striatum and cortex of BACHD/GFAP-CreERT2-tam mice.

55 phaB-crystallin in the striatum of the BACHD/GFAP-CreERT2 mice, indicating a cell autonomous effect o

56 Participants with baseline GFAP > 232pg/ml showed 160% faster decline in hippocampa

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

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

59 cell markers and expressed BDNF, TGF-beta1, GFAP, and IL-6.

60 Analysis of blood GFAP concentrations using prototype assays on a point-of

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

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

63 The number of SVZ stem cells (BrdU+GFAP+) was decreased in SNCA-A30P mice, whereas prolifer

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

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

66 FTIR and the glial distribution revealed by GFAP immunohistochemistry.

67 neuronal stem cells (iNSCs) were verified by GFAP.

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

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

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

71 lts demonstrated a temporal profile of CD68, GFAP, and HMGB1 after TBI relative to sham, which differ

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

73 Dunn Kruskal-Wallis test was used to compare GFAP concentrations between MRI lesion types with Benjam

74 observations that GFAP complexes containing GFAP variants are more resistant to solvent extraction.

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

76 We compare their capability of detecting GFAP in a clean-buffer and serum-matrix by using gold-co

77 each of whom carried a common but different GFAP mutation (R79C, R239H, or R416W).

78 For EV-GFAP, we observed 93% sensitivity, 38% specificity, 74%

79 17) of brain tumor patients showed higher EV-GFAP than the maximum observed in controls.

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

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

82 Glial fibrillary acidic protein expressing (GFAP(+)) glia modulate nociceptive neuronal activity in

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

84 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

85 AUC for GFAP in patients with CT-negative and MRI-positive findi

86 e was the area under the ROC curve (AUC) for GFAP in patients with CT-negative and MRI-positive findi

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

88 blastoma cell lines secrete EVs enriched for GFAP and Tau.

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

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

91 chemistry demonstrated positive staining for GFAP, Olig2, and a high Ki-67 proliferative index.

92 lop three different detection strategies for GFAP, among the most popular in the biosensing field and

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

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

95 In contrast, after GCI, GFAP-ARO-KO mice: (1) lacked the normal elevation of ast

96 tissues in human and mouse, and found a gene-GFAP-related to aging in both human and mouse.

97 IIbeta positive) and (46.63% +/- 2.5%) glia (GFAP positive), PPA treatment drastically shifted differ

98 Higher GFAP levels were associated with stroke severity and his

99 In the presymptomatic period, higher GFAP concentrations were correlated with a lower cogniti

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

101 , C3), TLR4, and colabeling with glia (IBA1, GFAP) were examined using gene expression, immunofluores

102 Deletion of Cav1.2 channels in GFAP-positive astrocytes during cuprizone-induced demyel

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

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

105 hich the Cav1.2 alpha subunit was deleted in GFAP-positive astrocytes.

106 We demonstrated that ACBP deletion in GFAP+ astrocytes, but not in Nkx2.1-lineage neural cells

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

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

109 -mediated recombination initiated gliomas in GFAP-FLPo mice.

110 ocytes exhibit a cell-autonomous increase in GFAP immunoreactivity without affecting astrocyte or mic

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

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

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

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

115 hat express FLPo recombinase specifically in GFAP-positive cells.

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

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

118 mtDNA, reduced MAP2 (neuronal) and increased GFAP (astrocyte) mRNA, relative to NCI.

119 mmatory cell infiltrate as well as increased GFAP and S100B co-expression and decreased HuC/D protein

120 entiation, we found that n-3 PUFAs increased GFAP expression and GFAP positive cell formation.

121 orsal horn, males and females show increased GFAP(+) astrocytic cells; however, only males demonstrat

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

123 epared from YAP 5SA-expressing cells induced GFAP(+) cell production in vitro, suggesting that a solu

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

125 Interestingly, GFAP levels in some patients with double-Ab-seronegative

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

127 RNA-seq) analysis revealed that the ischemic GFAP-ARO-KO mouse hippocampus failed to upregulate the "

128 "dorsal cap" received a mixed group of long GFAP- and vimentin-immunopositive processes from a dista

129 exit layer I, and "typical" ILA with longer GFAP(+) processes that exit layer I.

130 , and decreased phosphorylation of lysosomal GFAP, with no change in macroautophagy.

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

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

133 led by co-localization with the glial marker GFAP and absence of co-localization with the neuronal ma

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

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

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

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

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

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

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

141 rmining the relative levels of WT and mutant GFAP in three individuals with AxD, each of whom carried

142 n all three individuals, the level of mutant GFAP was less than that of the WT.

143 some toxic threshold rather than the mutant GFAP being inherently toxic.

144 s due to an intrinsic toxicity of the mutant GFAP instead of it acting indirectly by being more stabl

145 of GFAP in AxD patients is that the mutated GFAP variants are more stable than the WT, an attributio

146 paring its signal to that of an added [(15)N]GFAP standard.

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

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

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

150 is to evaluate the discriminative ability of GFAP for positive MRI scans in patients with negative CT

151 We assessed the discriminative ability of GFAP to identify MRI abnormalities in patients with norm

152 on and injury were pronounced, an absence of GFAP staining was consistent with activation-induced cel

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

154 A possible mechanism for accumulation of GFAP in AxD patients is that the mutated GFAP variants a

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

156 e of the disease is aberrant accumulation of GFAP.

157 t preventing or reducing the accumulation of GFAP.

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

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

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

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

162 gigaxonin is involved in the degradation of GFAP.

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

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

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

166 TDF also increased expression of GFAP and decreased expression of IBA1 in the wt and gp12

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

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

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

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

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 ayed by mice that express elevated levels of GFAP from a human WT GFAP transgene has contributed to t

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

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

176 rst, we found glial limitans injury, loss of GFAP immunostaining, and infiltration of T cells across

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

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

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

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

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

182 ogies which can be linked to the presence of GFAP in blood severely affect the human central nervous

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

184 rocytes resulted in both the upregulation of GFAP and cytokines that are associated with astrocyte ac

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

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

187 (GFAP) promoter-driven aromatase knock-out (GFAP-ARO-KO) mouse model to deplete astrocyte-derived E2

188 (GFAP) promoter-driven aromatase knock-out (GFAP-ARO-KO) mouse to deplete astrocyte-derived E2 and e

189 Plasma GFAP and neurofilament light chain (NfL) concentration w

190 Plasma GFAP concentration was significantly increased in sympto

191 Plasma GFAP concentrations (pg/mL) were measured using a protot

192 Median plasma GFAP concentration was highest in patients with CT-negat

193 ed to investigate the relationship of plasma GFAP to clinical and imaging measures.

194 Positive GFAP expression was detected in the control positive gro

195 of the YAP gene (YAP 5SA) causes productive GFAP(+) cell generation at late embryonic periods, and t

196 oding the intermediate filament (IF) protein GFAP.

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

198 (p < 0.05), glial fibrillary acidic protein (GFAP) (p < 0.05) in the cerebellum, and SYP (p < 0.05) a

199 (NF-L), and glial fibrillary acidic protein (GFAP) after elective cardiac surgery with the implementa

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

201 pression of glial fibrillary acidic protein (GFAP) and cellular hypertrophy.

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

203 Glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1(IBA

204 ve markers: Glial Fibrillary Acidic Protein (GFAP) and S100 Calcium-Binding Protein beta (S100beta);

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

206 ntration of glial fibrillary acidic protein (GFAP) and Tau.

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

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

209 ntration of glial fibrillary acidic protein (GFAP) correlates with intracranial injury visible on CT

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

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

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

213 ions in the glial fibrillary acidic protein (GFAP) gene.

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

215 Glial fibrillary acidic protein (GFAP) is a measure of astrogliosis, a known pathological

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

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

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

219 remodeling, glial fibrillary acidic protein (GFAP) promoter demethylation and a striking lengthening

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

221 generated a glial fibrillary acidic protein (GFAP) promoter-driven aromatase knock-out (GFAP-ARO-KO)

222 generated a glial fibrillary acidic protein (GFAP) promoter-driven aromatase knock-out (GFAP-ARO-KO)

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

224 (Nf-L), and glial fibrillary acidic protein (GFAP) with common sporadic Alzheimer disease (AD) and co

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

226 FL), S100B, glial fibrillary acidic protein (GFAP), amyloid-beta (Abeta) 40 and Abeta42, total tau (t

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

228 pression of glial fibrillary acidic protein (GFAP), and the upregulation of genes that have been prev

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

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

231 100beta and glial fibrillary acidic protein (GFAP), were used as indicator for neural differentiation

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

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

234 e developed glial fibrillary acidic protein (GFAP)-FLP recombinase (FLPo) mice that express FLPo reco

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

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

237 as well as glial fibrillary acidic protein (GFAP).

238 te filament glial fibrillary acidic protein (GFAP).

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

240 trations of glial fibrillary acidic protein (GFAP, p = 0.0074) and myelin basic protein (MBP, p = 0.0

241 Glial-fibrillary-acidic-protein (GFAP) has recently drawn significant attention from the

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

243 yte damage (glial fibrillary acidic protein [GFAP]) were measured.

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

245 Stereologic methods were used to quantify GFAP-immunoreactive astrocyte density and soma volume in

246 Raised GFAP concentrations appear to be unique to GRN-related F

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

248 continuous borders and significantly reduced GFAP density.

249 pendent phosphorylation of the CMA regulator GFAP.

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

251 Resident GFAP(+) glia in dorsal root ganglia (DRG) known as satel

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

253 OMCs express glial markers (p75(NTR), S100B, GFAP and oligodendrocyte marker O4), neuronal markers (n

254 Substance P (SP), S100beta, GFAP, and phosphorylated mitogen-activated protein kinas

255 er described rudimentary ILA that have short GFAP(+) processes that do not exit layer I, and "typical

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

257 t with prior experimental and human studies, GFAP, was highest at 6 h post-injury, while no substanti

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

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

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

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

262 an attribution abetted by observations that GFAP complexes containing GFAP variants are more resista

263 We show that GFAP-CreERT2 expression in these mice is highly selectiv

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

265 just prior to symptom onset, suggesting that GFAP may be an important marker of proximity to onset, a

266 The GFAP-ARO-KO mice exhibited significantly attenuated reac

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

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

269 osis, was significantly downregulated in the GFAP-ARO-KO hippocampus following GCI.

270 onal damage and microglial activation in the GFAP-ARO-KO mice after GCI, suggesting that the defects

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

272 Moreover, we found that the GFAP(+) cells were not YAP 5SA-expressing cells themselv

273 -expressing system, we demonstrated that the GFAP-FLPo mouse model enables the analysis of various st

274 GFAP-BDNF mice, which express BDNF under the GFAP promoter.

275 This GFAP level is compatible with clinical diagnostics.

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

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

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

279 duce AxD by increasing accumulation of total GFAP above some toxic threshold rather than the mutant G

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

281 han WT GFAP and thereby increasing the total GFAP level.

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

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

284 lent brain penetration, and efficacy in Tsc1(GFAP)CKO mice qualify 8 as a potential therapeutic candi

285 pal and LC microglial abundance, upregulated GFAP expression, degeneration of LC fibers, decreased st

286 ically activated astrocytes in the DMS using GFAP promoter-driven expression of hM3Dq, the excitatory

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

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

289 ein levels were increased after mTBI as were GFAP and IBA-1 markers.

290 ntin- and nestin-immunopositive glia whereas GFAP and the water-channel aquaporin 4 were found at the

291 ts, reovirus antigen did not colocalize with GFAP in infected brains, suggesting that reovirus does n

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

293 ional mHTT-expressing BACHD mouse model with GFAP-CreERT2 mice.

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

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

296 on of the L-type amino acid transporter with GFAP-positive astrocytes but not CD68-positive microglia

297 ress elevated levels of GFAP from a human WT GFAP transgene has contributed to the notion that the mu

298 ified a peptide specific to the mutant or WT GFAP in each patient, and we quantified this peptide by

299 ting indirectly by being more stable than WT GFAP and thereby increasing the total GFAP level.

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