ライフサイエンスコーパス: glial

1 lattice-like organization is also found for glial actin.

2 lum and spinal cord that was consistent with glial activation and increased T-cell, monocyte, and neu

3 n (paradigm A) reversed the diabetes-induced glial activation and loss of function of amacrine cells

4 The selective glial activation in tissues from GFAP::hM3Dq mice evoked

5 Glial activation in white matter assessed by translocato

6 Such glial activation may have negative implications for the

7 how Draper is cell autonomously required for glial activation of transcriptional reporters after axon

8 phine conditioning, reduces morphine-induced glial activation, and increases microglial expression of

9 multiparous mice had smaller infarcts, less glial activation, and less behavioral impairment in the

10 haracterized by CNS infiltration of T cells, glial activation, and progressive loss of motor function

11 he translocator protein (TSPO), a marker for glial activation, have yielded inconsistent results.

12 response through its role in downregulating glial activation, however, the intact apoE holoprotein d

13 upper-respiratory viral infection can cause glial activation, promote immune cell trafficking to the

14 ovided neuroprotective effects and inhibited glial activation, suggesting that chrysophanol might hav

15 amage often triggers neuronal cell death and glial activation, with very limited spontaneous axon reg

16 euronal degeneration in RP is exacerbated by glial activation.

17 e neuronal dysfunction and loss, and chronic glial activation.

18 We used transgenic mice to modify glial activity and found that enteric glia significantly

19 Together, our findings show that glial activity contributes to the regulation of electrog

20 ribute to the neurogenic ion transport while glial activity does not appear to play a major role in t

21 The selective activation of glial activity evoked electrogenic ion transport primari

22 to analyze the nanoscale organization of 12 glial and axonal proteins at the nodes of Ranvier of tea

23 ence of gene expression changes in neuronal, glial and endothelial cell-types, which enabled predicti

24 These drugs could restore glial and glymphatic function, enabling efficient draina

25 overall reduction is due to decreased radial glial and granule neuron progenitor cell proliferation.

26 ich consisted primarily of neurons with some glial and neural progenitor cells.

27 cal conditions, this review will outline the glial and neuroimmune mechanisms that may contribute to

28 lar glycine by blocking either, or both, the glial and neuronal glycine transporters markedly decreas

29 ate enhancer activity and NFIA expression in glial and neuronal populations.

30 ollower-axon guidance, respectively, and for glial and pioneer-neuron Flamingo (CELSR) in follower-ax

31 ohistochemistry to cells positive for neural/glial antigen 2 (NG2) expressed in hepatic pericytes, gl

32 velopmental origin (Tbr1, Sp8), and neuronal/glial antigens for phenotype characterization.

33 We report here that glial App plays a role in physiology and in the regulati

34 A few nodes were devoid of glial apposition.

35 Rotenone produced no significant changes in glial ATP levels.

36 R) is prominently dysregulated in high-grade glial brain tumors, blockade of PI3K or AKT minimally af

37 ::CreER(T2+/-) /Cx43(f/f) mice or activating glial calcium responses in GFAP::hM3Dq mice, and tested

38 studies have suggested that it also inhibits glial cell activation in rodents, and may alter opioid-m

39 enzyme expression, fragmented mitochondria, glial cell activation, muscle atrophy, weight loss, and

40 ut there has been little study of persistent glial cell activity in brains of athletes with sports-re

41 KEY POINTS: The role of enteric glial cell activity in the acute regulation of epithelia

42 But whether glial cell activity regulates these functions acutely un

43 ncase the motor nerve despite this change in glial cell and myelin composition, remains unknown.

44 day 16 of differentiation, in the absence of glial cell co-culture.

45 AT1-, STAT2-, or IRF9-deficient murine mixed glial cell cultures (MGCs).

46 em (e.g., neurogenesis, synaptic plasticity, glial cell development) and immune functions (e.g., immu

47 in tissue pathology, including inflammation, glial cell dysfunction, and angiogenesis, its role in th

48 ced reelin signaling and disorganized radial glial cell fibers.

49 , we examined the effects of BNN27 on neural/glial cell function, apoptosis, and inflammation in the

50 haII-spectrin breakdown products, SBDPs) and glial cell injury biomarker, glial fibrillary acidic pro

51 he first systematic quantitative analysis of glial cell insertions at central nodes of Ranvier.

52 Glial cell line-derived neurotrophic factor (GDNF) binds

53 rophic effects, the therapeutic potential of glial cell line-derived neurotrophic factor (GDNF) has b

54 , we describe a novel, biphasic function for glial cell line-derived neurotrophic factor (GDNF) in th

55 m.SIGNIFICANCE STATEMENT Delivery of ectopic glial cell line-derived neurotrophic factor (GDNF) promo

56 we evaluate the differential potency of NGF, glial cell line-derived neurotrophic factor (GDNF), brai

57 We also found that intraspinally expressed glial cell line-derived neurotrophic factor (GDNF), but

58 anscription factors Distal-less 3 (DLX3) and Glial cell missing-1 (GCM1) have been shown to coordinat

59 nitor cells (OPCs), the resident myelinating glial cell of the CNS, into the periphery.

60 lls or polydendrocytes, which are a resident glial cell population in the mature mammalian central ne

61 iated hemichannel activity specifically in a glial cell population.

62 ZIKA-NS2A, but not DENV-NS2A, reduces radial glial cell proliferation and causes AJ deficits in human

63 protein 18 kDa (TSPO), a marker of activated glial cell response, in a cohort of National Football Le

64 ion with structural changes in astrocytes, a glial cell that influences neural communication.

65 Despite the importance of this heterogeneous glial cell type for brain development and function, the

66 ression is essential for proper neuronal and glial cell type specification.

67 served early and mature cortical neurons and glial cell types produced late.

68 ive tissue comprised of six neuronal and one glial cell types, each of which develops in prescribed p

69 t dysfunction of astrocytes, a major type of glial cell, leads to neuronal vulnerability.

70 Here we identify glial cell-derived neurotrophic factor (GDNF) receptor a

71 The ability of the HS-binding neuropeptide glial-cell-line-derived neurotrophic factor (GDNF) to in

72 NG2(+) glial cells (also called oligodendrocyte progenitors or

73 GFAP and other markers of enteric glial cells (eg, p75 and S100B), colocalized with gastri

74 Radial glial cells (RGCs) are the most abundant macroglia in th

75 Thanks to the persistence of radial glial cells acting as neural stem cells, the brain of th

76 ediated by rabconnectin-3alpha in neurons or glial cells afferent to GnRH neurons.

77 of infected cells in the visual system were glial cells along the optic tract.

78 tion and premature differentiation of radial glial cells and aberrant positioning of newborn neurons.

79 allin, a protein that is expressed mainly in glial cells and mediates exosome secretion.

80 mesenchyme, differentiated into neurons and glial cells and showed neuronal activity, as measured by

81 a commonly used sedative, pentobarbital, on glial cells and their uptake of nanoparticles.

82 TSPO is upregulated in glial cells and used as a measure of neuroinflammation i

83 se mutation (S140G), neurons accumulate, and glial cells are dispersed along the rostral migratory st

84 the primary immune responders in the brain, glial cells are implicated as key players in the onset a

85 field (SMF) on Central Nervous System (CNS) glial cells are less investigated.

86 ABSTRACT: Enteric glial cells are often implicated in the regulation of ep

87 ucose from the blood and lactate produced by glial cells as sources of energy.

88 tion of surface receptors within neurons and glial cells by affecting their delivery to lysosomes for

89 in, demonstrating that, although perineurial glial cells display plasticity despite myelin perturbati

90 ance and exaggerated release of glutamate by glial cells during immune activation leads to glutamate

91 bleaching and photoconversion experiments in glial cells expressing vimentin, glial fibrillary acidic

92 Primary enteric glial cells from C57BL/6 mice were incubated with gastri

93 Evidence suggests glial cells have an essential and underappreciated role

94 After traumatic brain injury (TBI), glial cells have both beneficial and deleterious roles i

95 neuron cultures is possible, the removal of glial cells ignores physiologically relevant cell-cell i

96 Astrocytes are the most common glial cells in the brain with fine processes and endfeet

97 a) is essential for migration of neurons and glial cells in the developing mouse brain.

98 and it causes cell-cycle deficits of radial glial cells in the embryonic mouse cortex and human fore

99 Astrocytes, the most abundant glial cells in the mammalian brain, are critical regulat

100 d mouse primary astrocytes and in Drosophila glial cells in vivo.

101 ute phase of TBI management, their effect on glial cells is not well understood.

102 overexpression of sEH in the retinal Muller glial cells of non-diabetic mice resulted in similar ves

103 ly was found in the cytoplasm of neurons and glial cells of the prefrontal cortex at 4 and 24 hours p

104 Glial cells offer protection against AD by engulfing ext

105 For instance, enteric glia, a collection of glial cells residing within the walls of the intestinal

106 Our findings emphasize the ability of glial cells such as OPCs to positively respond to modera

107 lectively enriched in subsets of neurons and glial cells that degenerate in ALS.

108 Oligodendrocytes are glial cells that populate the entire CNS after they have

109 Enteric glial cells that stained positive for glial fibrillary a

110 p in the submucosa, might arise from enteric glial cells through hormone-dependent PKA signaling.

111 pathway that affects the critical support of glial cells to neurons in the HD brain.

112 sion, explaining the apparent sensitivity of glial cells to Pico/Ras(V12) overexpression.

113 N1 is mostly expressed by neurons and not by glial cells under normal conditions, similar to the expr

114 is, meningitis, and meningoencephalitis, and glial cells were identified as principal targets of infe

115 Primary glial cells were incubated with leptomycin b and MG132 t

116 Astrocytes are complex glial cells with numerous fine cellular processes that i

117 We focused on neurons and glial cells within the olfactory bulb because the virus

118 Highly specialized glial cells wrap axons with a multilayered myelin membra

119 ells, their antineuroinflammatory effects on glial cells, and the ability to ameliorate nesting behav

120 basic unit in the brain, including neurons, glial cells, blood vessels and extracellular matrix.

121 al mediated by gliotrophic FGF signaling.How glial cells, such as astrocytes, acquire their character

122 n two processes that require phagocytosis by glial cells, the immune cells in the brain: neuronal cle

123 gulation when its function is manipulated in glial cells.

124 acroautophagy, and in some cases transfer to glial cells.

125 rectifying K(+) channel Kir4.1 in satellite glial cells.

126 onomously assembled by these axon-associated glial cells.

127 and lytic infection by neurotropic JCPyV in glial cells.

128 rectifying K(+) channel Kir4.1 in satellite glial cells.

129 ify and measure specific types of neurons or glial cells.

130 igment epithelium and for neighboring Muller glial cells.

131 tatory and inhibitory neurons, as well as in glial cells.

132 stricted to two populations of Repo-positive glial cells: an invasive population, characterized by JN

133 including pre- and post-synaptic neurons and glial cells; 60 papers were included in this review.

134 The mixed glial cellular model may be useful in developing therape

135 The SCZ glial chimeras also showed delayed astrocytic differenti

136 Our approach was to establish humanized glial chimeric mice using glial progenitor cells (GPCs)

137 MMP-1 as a novel cascade required for proper glial clearance of severed axons.

138 of pre-OLs is an integral component of axon-glial communication and is required for the function and

139 Oligodendrocyte (OL) maturation and axon-glial communication are required for proper myelination

140 ing properties of OLs and their role in axon-glial communication in the auditory brainstem.

141 aturation of OLs to promote myelination.Axon-glial communication is important for myelination.

142 chondrial dysfunction in which primary mixed glial cultures (astrocytes, microglia and oligodendrocyt

143 Primary enteric glial cultures were generated from the VillinCre:Men1(FL

144 Our results show that the reduction of glial Cx43 expression in Sox10::CreER(T2+/-) /Cx43(f/f)

145 athological hallmark is the oligodendrocytic glial cytoplasmic inclusion (GCI) consisting of alpha-sy

146 lein aggregates in oligodendrocytes, forming glial cytoplasmic inclusions.

147 the prominent neuronal migration and radial glial defects in hippocampus and cortex seen in double-K

148 ing depolarization is a wave of neuronal and glial depolarization.

149 n of Ret, a receptor tyrosine kinase for the glial derived neurotrophic factor (GDNF) family ligands

150 We had previously found that glial derived neurotrophic factor (GDNF) is reduced in S

151 Because glia and glial-derived growth cone repellent factors (especially

152 The cellular basis for neuronal versus glial determination in progenitors involves asymmetric p

153 e report that certain aspects of perineurial glial development and injury responses are mostly unaffe

154 ripheral motor axons, we assayed perineurial glial development, maturation, and response to injury.

155 r-beta1 as a partial mediator of perineurial glial development.

156 progenitor cells (hGPCs) revealed disrupted glial differentiation-associated and synaptic gene expre

157 ar developmental hierarchies and lineages of glial differentiation.

158 imilar expansion of cells that lack terminal glial differentiation.

159 tant animals, whereas enhanced expression of glial Draper reverses Abeta accumulation, as well as beh

160 eurogenic ion transport with veratridine and glial driven responses consisted of both tetrodotoxin-se

161 his study, we investigated whether intrinsic glial dysfunction contributes to the pathogenesis of sch

162 This is the first report demonstrating that glial dysfunctions could contribute to nonsyndromic auti

163 ranscriptome in addition to various types of glial, endothelial, and blood cells.

164 Here, we show that the highly conserved glial engulfment receptor Draper/MEGF10 provides neuropr

165 alphaSNAP phenotypes, which included loss of glial ensheathment of neuron cell bodies, increased neur

166 This work identifies essential roles for glial ensheathment of neuronal cell bodies in CNS homeos

167 he activity of enteric glia, either reducing glial expression of connexin 43 in Sox10::CreER(T2+/-) /

168 iological signals regulating neuronal versus glial fate are largely unknown.

169 in impaired AJ formation and aberrant radial glial fiber scaffolding in the embryonic mouse cortex.

170 b1 depletion favors NSC differentiation into glial fibrillar acidic protein (GFAP)-immunoreactive cel

171 ice had a sharp increase in the glial marker glial fibrillary acidic protein (GFAP) and in Slit2 at t

172 ascular endothelial growth factor (VEGF) and glial fibrillary acidic protein (GFAP) expressions were

173 the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP) lead to the rare

174 BACKGROUND & AIMS: When the glial fibrillary acidic protein (GFAP) promoter is used

175 rs S100B, neuron-specific enolase (NSE), and glial fibrillary acidic protein (GFAP), in addition to m

176 The expression patterns of S100beta and glial fibrillary acidic protein (GFAP), were used as ind

177 cts, SBDPs) and glial cell injury biomarker, glial fibrillary acidic protein (GFAP)-breakdown product

178 e central nervous system (CNS) disorder with glial fibrillary acidic protein (GFAP)-IgG as biomarker

179 nteric glial cells that stained positive for glial fibrillary acidic protein (GFAP+) expressed gastri

180 in, levels of RAGE and Toll-like receptor 4, glial fibrillary acidic protein and neuronal nitric-oxid

181 ice were able to increase astrocyte-produced glial fibrillary acidic protein in the hippocampus, whic

182 e)-loxP system under regulation of the mouse glial fibrillary acidic protein promoter to knock out th

183 ium binding adaptor molecule 1), astrocytes (glial fibrillary acidic protein), and neuronal nuclei we

184 a pointed star, especially when visualizing glial fibrillary acidic protein, a canonical marker for

185 nized calcium-binding adapter molecule 1 and glial fibrillary acidic protein, and behavioral deficits

186 eriments in glial cells expressing vimentin, glial fibrillary acidic protein, and nestin, we show tha

187 be recognized as such by their expression of glial fibrillary acidic protein, glutamine synthetase, g

188 retinal tissues using immunofluorescence for glial fibrillary acidic protein, microglia-specific prot

189 ies showed that postnatal ablation of LPL in glial fibrillary acidic protein-expressing astrocytes in

190 stry, GluR2-immunocytochemistry, Timm stain, glial fibrillary acidic protein-immunocytochemistry, glu

191 luorescence for AQP4, amyloid-beta 1-42, and glial fibrillary acidic protein.

192 unlike injury-reactive ones, did not express glial fibrillary acidic protein.

193 associate glutamate recycling, sleep, and a glial function for the App family proteins.SIGNIFICANCE

194 However, perineurial glial function is disrupted along nerves containing cent

195 here is growing evidence that disruptions in glial function may be implicated in numerous neurologica

196 the effect of peripheral surgery on neuronal-glial function within hippocampal neuronal circuits of r

197 better understand the roles of microRNAs in glial function, we used a conditional deletion of Dicer1

198 Most glial functions depend on establishing intimate morpholo

199 description of the impact of inflammation on glial glutamate regulation at the cellular, molecular, a

200 aspartate transporter levels were higher and glial glutamate transporter 1 levels were lower in the D

201 SLC1A3 encodes the glial glutamate transporter hEAAT1, which removes glutam

202 reduce axonal glutamate release and increase glial glutamate uptake.

203 the IL-1beta-dependent downregulation of the glial glutamate-aspartate transporter (GLAST), which cau

204 rgic currents dominate, blocking neuronal or glial glycine transporters enhances tonic glycinergic cu

205 (CNS) spatial domains that actively restrict glial growth, and selective ablation of cortex glia caus

206 onal programs governing these complex innate glial immune responses are still unclear.

207 Interestingly, glial induction of MMP-1 requires the highly conserved e

208 vent motor neuron cell death, but it reduced glial inflammation and blocked activation of the stress-

209 cell infiltration to the nigra and incessant glial inflammation.

210 ardized neuroprotection protocols that limit glial injury could significantly improve intact survival

211 on microscopy confirmed the presence of dual glial insertion at some nodes and further revealed that

212 eview, we consider recent insights into axon-glial interactions during development and disease to pro

213 In sum, this review will argue that neural-glial interactions represent an important avenue for adv

214 that are proposed to be critical to neuronal-glial interactions through the mediator SNa.

215 fic cell adhesion molecule that promotes axo-glial interactions.

216 Expression levels of glial intermediate filaments (GFAP, vimentin) and extrac

217 double-pronged blockage of T3 action during glial lineage commitment.

218 novel disease mechanism and the finding that glial lipid metabolism is critical for axon function, in

219 ing series double immunostained for a radial glial marker (BLBP) and cell proliferation marker (PCNA)

220 NgR123-null mice had a sharp increase in the glial marker glial fibrillary acidic protein (GFAP) and

221 ress both Nestin and p75NTR, but not the pan-glial marker Sox10.

222 therefore suggest a causal role for impaired glial maturation in the development of schizophrenia and

223 riggers swift responses from glia, including glial migration and phagocytic clearance of damaged neur

224 y as essential for the maintenance of cortex glial morphology and continued contact with neurons.

225 ng factor required for maintenance of cortex glial morphology and neuron-glia contact.

226 wed that LIF promoted the differentiation of glial nerve sheath Schwann cells and induced their migra

227 exploit this bottleneck to define roles for glial Netrin and Semaphorin in pioneer- and follower-axo

228 An axoglial adhesion complex comprising glial Neurofascin155 and axonal Caspr/Contactin flanks m

229 restored by FKBP1b associated primarily with glial-neuroinflammatory, ribosomal, and lysosomal catego

230 The expression patterns of specific glial, neuronal, and inflammatory molecules were evaluat

231 characterized by increased expression of the glial nexin Serpine2, the human ortholog, which was incr

232 In contrast, axonal and glial nodal adhesion molecules [neurofascin-186, neuron

233 arkers Sox2 and Nestin, and lacks markers of glial or neuronal differentiation.

234 fully viable in the absence of any signs of glial or neuronal loss, suggesting that astrocytes are n

235 We conclude that succinate can improve glial oxidative metabolism, consistent our previous find

236 peration of P2X7Rs at neurons, more recently glial P2X7Rs are increasingly considered as indirect cau

237 an extended period of time in the absence of glial pathology or unspecific signs of neurodegeneration

238 nd synaptic gene expression, indicating that glial pathology was cell autonomous.

239 0.001], cell body [p = 0.003], and neuritic/glial-processes [p = 0.004]).

240 imic in vivo temporal patterns of neuron and glial production, with immature progenitors and neurons

241 stablish humanized glial chimeric mice using glial progenitor cells (GPCs) produced from induced plur

242 RNA-seq of cultured SCZ human glial progenitor cells (hGPCs) revealed disrupted glial

243 ghly elongated basal processes of the radial glial progenitor cells and impairment of postmitotic neu

244 Cell, Windrem et al. (2017) transplant human glial progenitors from schizophrenia patients into mouse

245 Individual radial glial progenitors in the developing thalamus actively di

246 ng from low-titre retrovirus-infected radial glial progenitors in the embryonic medial ganglionic emi

247 stigated the effect of Abeta on neuronal and glial proliferation by using an APP/PS1 transgenic model

248 axonal proteins (betaII spectrin, Caspr) and glial proteins (neurofascin-155, ankyrin B) form periodi

249 e between the position of the axonal and the glial proteins.

250 cal handle, we selectively label neuronal or glial proteomes.

251 ignificant decrease of retinal thickness and glial reactivity was observed without an increase in apo

252 but the repertoire of molecules required for glial recognition and destruction of Abeta are still unc

253 Glial recordings confirmed EAAT2 is functional on nTS as

254 These transcripts also include glial regulators of synaptic refinement, such as Sparc F

255 adhesion molecules [neurofascin-186, neuron glial-related cell adhesion molecule (NrCAM)] can arrang

256 mination of the treatment and did not induce glial remodelling in the brain.

257 flammatory model that allows the analysis of glial responses in MS, we show that endogenous CRYAB exp

258 in adult Drosophila that elicits widespread glial responses in the ventral nerve cord (VNC).

259 euroepithelial (NE) cells differ from radial glial (RG) cells in both primary tissue and in stem cell

260 r, our studies reveal previously undescribed glial roles in pioneer-axon guidance, suggesting conserv

261 midal neurons and malformation of the radial glial scaffold, akin to the hippocampal lamination defec

262 lized fibrotic scar surrounded by a reactive glial scar at the lesion site.

263 ctive, we discuss the divergent roles of the glial scar during CNS regeneration and explore the possi

264 nd tissue is suspected to be a key driver of glial scar formation around neural implants.

265 bility of soft hydrogel coatings to modulate glial scar formation by reducing local strain.

266 cytokines leads to dramatic inflammation and glial scar formation, affecting brain tissue's ability t

267 on regeneration, beneficial functions of the glial scar have also been recently identified.

268 Glial scar is a significant barrier to neural implant fu

269 The glial scar was also altered in the absence of acutely di

270 One such response, the glial scar, is a structural formation of reactive glia a

271 tional heterogeneity within the cells of the glial scar-specifically, astrocytes, NG2 glia and microg

272 ate in large numbers among astrocytes in the glial scar.

273 not be the main CSPG contributory factor in glial scar.

274 ar composition of neural tissue and leads to glial scarring, which inhibits the regrowth of damaged a

275 Mammalian glial scars supposedly form a chemical and mechanical ba

276 glia largely segregate into the fibrotic and glial scars, respectively; therefore, we used a thymidin

277 rs of chromaffin cells arise from peripheral glial stem cells, termed Schwann cell precursors (SCPs).

278 The selective glial stimulation did not affect transmural ion conducta

279 ne in the absence of the floor plate (FP), a glial structure occupying the midline.

280 Astrocytes are the most populous glial subtype and are critical for brain function.

281 Results showed a neuronal and glial tau accumulation in granulin mutation cases.

282 aining revealed neuronal pretangle forms and glial tau in both astrocytes and oligodendrocytes.

283 Neuronal and glial tau lesions comprised of 4-repeat isoforms in brai

284 d mice showed spatiotemporal transmission of glial tau pathology, suggesting glial tau transmission c

285 ry tangles and Pick bodies and in some cases glial Tau pathology.

286 nsmission of glial tau pathology, suggesting glial tau transmission contributes to the progression of

287 ioid-based pain management via inhibition of glial TLR4 and illustrate the necessity for sex-specific

288 nated fewer glia but caused considerable non-glial toxicity and epithelial cell death.

289 quires enteric glia can be attributed to non-glial toxicity in Gfap(HSV-TK) mice and epithelial-cell

290 ct is absent in slices treated with either a glial toxin or an adenosine A1 receptor antagonist.

291 d be manipulated to repair myelin in lieu of glial transplantation.

292 myelination, and clinical trials have tested glial transplants to promote myelin repair.

293 ate-aspartate transporter (GLAST), a crucial glial transporter involved in glutamate homeostasis.

294 maintained their honeycomb organization and glial tubes.

295 provide useful information for preoperative glial tumor grading.

296 4 females) with histopathogical diagnosis of glial tumor undergoing routine cranial MRI, SWI, and per

297 distinguish between high-grade and low-grade glial tumors.

298 e with oncogenic Ras to promote formation of glial tumours, and that, in this context, Mal/serum resp

299 , lung (H460), skin (A431), neuronal (BE2C), glial (U87, SJG2), and pancreatic (MIA) cancers.

300 group in NAC is required for its effects on glial viability and protein quality control.

301 ry acidic protein (GFAP) and in Slit2 at the glial wedge and indusium griseum, midline structures req