ライフサイエンスコーパス: brain cell

1 ion at the level of cell-cell contacts among brain cells.

2 n metabolism of glucose and ketone bodies in brain cells.

3 ells led to the identification of individual brain cells.

4 ause CRT is required for creatine entry into brain cells.

5 pid-lowering drugs, in up-regulating TPP1 in brain cells.

6 fibroblasts, cervical cancer HeLa cells, and brain cells.

7 lic AMP, a key second messenger available in brain cells.

8 taining sialic acid-independent binding with brain cells.

9 and decreases Abeta(42) toxicity in primary brain cells.

10 ng potential binding of mhIL-13-PE to normal brain cells.

11 gered by ascorbate stimulation in kidney and brain cells.

12 assemble into ordered aggregates in affected brain cells.

13 and binding to IL4R/IL13R, present in normal brain cells.

14 zed to impede turnover of folded proteins in brain cells.

15 of mhtt protein aggregates in both islet and brain cells.

16 proinflammatory cytokines and chemokines in brain cells.

17 rous medium formed by the spaces between the brain cells.

18 ar transport mechanisms not present in other brain cells.

19 ressed in normal brain cells nor in tumorous brain cells.

20 (h) CMVs in developing and mature brain and brain cells.

21 erences in sex chromosome gene expression in brain cells.

22 ction of meningioma, astrocytoma, and normal brain cells.

23 s of astrocytes or freshly dissociated fetal brain cells.

24 ay function as a growth suppressor in normal brain cells.

25 s using transfected L cells or primary chick brain cells.

26 f alpha-synuclein protein (alpha-syn) inside brain cells.

27 n from ischemic injury by acting directly on brain cells.

28 known as amyloid found inside and outside of brain cells.

29 eraction could mediate cell adhesion between brain cells.

30 ectly compare them to purified primary human brain cells.

31 ical neurons closely resembled primary fetal brain cells.

32 role in the tonic regulation of surrounding brain cells.

33 for functional studies upon NIR exposure to brain cells.

34 r routine non-inflammatory clearance of dead brain cells.

35 gical resection while sparing normal healthy brain cells.

36 etinoic acid is capable of enhancing TFEB in brain cells.

37 roglia and is thought to phagocytose damaged brain cells.

38 phocytes should reflect variation present in brain cells.

39 of neurons, as compared with other types of brain cells.

40 ng cell-to-cell communication, using primary brain cells, a microfluidic device, and a multiparametri

41 We show that apoptosis of a variety of brain cells after pneumococcal infection arises from inh

42 t important roles for the PMRS in protecting brain cells against age-related increases in oxidative a

43 ich scavenges complement fragments, protects brain cells against the deleterious effects of experimen

44 oblastoma cells in Matrigel and spheroid-rat brain cell aggregate models.

45 However, male and female brain cells also differ in genetic sex; thus, sex chromo

46 /- 4 mm(3); n = 14), indicating the resident brain cells also play a role.

47 Thirty percent of genes with DS-DM in adult brain cells also show DS-DM in fetal brains, indicating

48 emented creatine would be widely taken up by brain cells, although possibly less by those cells that

49 etween the processes responsible for loss of brain cells and beta-cells in these diseases.

50 antially larger than the size and spacing of brain cells and blood vessels, is injurious and triggers

51 target cell generation including stem cells, brain cells and cardiac cells.

52 g mechanism is electrical activity of single brain cells and cell assemblies.

53 no or negative effects of these compounds on brain cells and cognition have been found.

54 tituent in brain, is actively metabolized in brain cells and contributes to glutamine in the intersti

55 c transcripts initiated by P(N) and P(NN) in brain cells and fibroblasts, respectively.

56 in distinct populations of postmortem human brain cells and further our understanding of the regulom

57 yme gamma-secretase showed reduced damage to brain cells and improved functional outcome in a model o

58 R-339-5p regulates BACE1 expression in human brain cells and is most likely dysregulated in at least

59 he relative contribution of iNOS in resident brain cells and peripheral leukocytes infiltrating the i

60 n sleep and wake pooled transcripts from all brain cells and showed that several genes expressed at h

61 ffering capacity under ex vivo conditions in brain cells and slices.

62 ecord in awake humans the activity of single brain cells and small cellular assemblies.

63 etection of glucose concentration changes by brain cells and subsequent release of orexigenic or anor

64 s; and (3) localizing proteasome subunits in brain cells and synapses.

65 the primary source of brain-derived Hp among brain cells and that oligodendroglia-released Hp plays p

66 ain cells more easily than it infects mature brain cells and that this preference is independent of t

67 -104 cells induce to murine normal and tumor brain cells and their trafficking patterns in both norma

68 asses the release of protein aggregates from brain cells and their uptake by neighboring cells.

69 ecretory protein profile distinct from other brain cells and to modulate microglial activation, proli

70 nflammatory mediators by statins in cultured brain cells, and in central nervous system of EAE animal

71 ific mRNAs in developing male germ cells and brain cells, and is implicated in DNA recombination and

72 ated in membranes of retinal photoreceptors, brain cells, and testis, where it mediates transport of

73 m the perspective of neurons, extra-neuronal brain cells, and the systemic environment and highlight

74 hat are the consequences of staying awake on brain cells, and why is sleep needed?

75 indicate that AIF may play a central role in brain cell apoptosis and bacterial pathogenesis.

76 ing factor-dependent (AIF-dependent) form of brain cell apoptosis.

77 brain barrier is formed and postnatally when brain cells are amenable to culturing.

78 e suggest an alternate view: that developing brain cells are inherently more susceptible to CMV infec

79 dents suggest, however, that male and female brain cells are intrinsically different also because of

80 Although most brain cells are postmitotic, small populations of progen

81 Normally, brain cells are resistant to Shiga toxin (Stx), the puta

82 erular preparations were not contaminated by brain cells (astrocytes, oligodendrocytes, or neurons),

83 We deleted the Mecp2 gene in ~80% of brain cells at three postnatal ages to determine whether

84 ger and longer-term effort to generate whole-brain cell atlases in species including mice and humans.

85 Together, these data demonstrate that human brain cells (both neurons and non-neuronal cells) can be

86 Beta-amyloid (Abeta) has adverse effects on brain cells, but little is known about its effects on th

87 inked proteins confer stress on all relevant brain cells, but region-specific susceptibility stems fr

88 es activation of antiapoptotic mechanisms in brain cells by acting directly on endothelium and neuron

89 in Drosophila, in which remote activation of brain cells by genetic means enables us to examine the n

90 a commonly used antibiotic protects cultured brain cells by reducing viral proliferation.

91 n-Darby canine kidney) or endothelial (human brain) cells, by limited proteolysis with trypsin.

92 ul genetic tools available, small subsets of brain cells can be reliably manipulated, offering enormo

93 of per1 cells, which unlike other mammalian brain cells can survive and function at depolarized stat

94 elds, generated by the cooperative action of brain cells, can influence the timing of neural activity

95 Mammalian brain cells cannot synthesize riboflavin and must import

96 pair is required for neural development, and brain cells contain somatic genomic variations.

97 differences indicate that the genetic sex of brain cells contributes to the process of sexual differe

98 o release glutamate, which kills surrounding brain cells, creating room for tumor expansion.

99 induced demyelination in a three-dimensional brain cell culture assay.

100 lt in more cell death and apoptosis in fetal brain cells cultured in vitro.

101 ormed on total RNA isolated from adult mouse brain, cells cultured from P1 mouse cortex or meninges,

102 whether Fas functions as a death receptor in brain cells, cultured embryonic day 17 cortical neurons

103 rocytes as the major antioxidant producer in brain cell cultures exposed to HSV-1 stimulated microgli

104 e lactic acidosis of brain tissue leading to brain cell damage.

105 urrent moderate hypoglycemia had 62-74% less brain cell death and were protected from most of these c

106 tional methods using histopathology estimate brain cell death at a time remote from ischemic insult.

107 cocyte infiltration into the choroid plexus, brain cell death, and deficits in motivated behavior.

108 trix signaling and homeostasis, MMPs trigger brain cell death.

109 Heme deficiency in brain cells decreases mitochondrial complex IV, activate

110 nd the cerebellum, which points to potential brain cell dedifferentiation.

111 orts is also important for understanding how brain cells derived from diverse human genetic backgroun

112 Here, we review the molecular properties of brain cells derived from patients with neurodegenerative

113 of intact Cln1(-/-) mice as well as cultured brain cells derived from these animals with a thioestera

114 abundantly expressed in specific individual brain cells, despite being hard to detect in bulk sample

115 FGFR1 affects brain cell development by two distinct mechanisms.

116 ate insecticide, chlorpyrifos (CPF), impairs brain cell development, axonogenesis and synaptogenesis.

117 After uterine ischemia, certain fetal brain cells die immediately, and other cells undergo ong

118 tes versus ovaries), we found that XY and XX brain cells differed in phenotype, indicating that a bra

119 In response to ischemia, damaged/necrotic brain cells discharge factors that polarize MPhi to a M1

120 enlarged brains with an increased number of brain cells, displaying marked runting and developmental

121 ify regulatory elements that drive conserved brain cell diversity.

122 omas have telomerase activity whereas normal brain cells do not.

123 bral ischemia, and refers to the swelling of brain cells due to the entry of water from the extracell

124 A picture is emerging to suggest that brain cells, due to their nonproliferative nature, may b

125 ab1) functions in positional organization of brain cells during development.

126 fication is coupled to a gradual decrease in brain cell energy metabolism and increase in lipid perox

127 monemia have shown that ammonium is toxic to brain cells especially astrocytes and neurons.

128 of the genes coding for SOCS-3 and PTP-1B in brain cells, examined their sensitivity to hormone actio

129 omponents remained within these perivascular brain cells for at least 2 days.

130 The lack of live human brain cells for research has slowed progress toward unde

131 virus to induce proinflammatory signals from brain cells for the recruitment of blood-derived inflamm

132 roup comparisons of normal and disease model brain cells for the whole brain at a high spatial resolu

133 ning is critical for neural development, and brain cells frequently contain somatic genomic variation

134 ing hematoma absorption and protecting other brain cells from ICH-induced damage.

135 ion-induced apoptosis is reduced in cortical brain cells from MAO A-deficient mice compared with WT.

136 First, aneuploidy was found in brain cells from MAPT mutant transgenic mice expressing

137 TLD, we measured aneuploidy and apoptosis in brain cells from patients with MAPT mutations and identi

138 tPA shifts the apoptotic signal in stressed brain cells from the intrinsic to the extrinsic pathway

139 hich glucose and oxygen are delivered to the brain cells from the vascular system.

140 the interferon pathway protects normal human brain cells from VSV infection while maintaining the vul

141 ated, although to a lower degree than in the brain cells from which they were derived.

142 d plexus, rich sources of dendritic cells in brain, cells from retina may better represent the APC ac

143 rive one kind of specialized cell (such as a brain cell) from another, more accessible, tissue (such

144 u inclusions form first in a small number of brain cells, from where they propagate to other regions,

145 ISG15 protein modification is essential for brain cell function.

146 tiated stem cells are recovered in which the brain cell genome has undergone epigenetic reprogramming

147 ine (hmC) maps revealed that hmC marks fetal brain cell genomes at putative regulatory regions that a

148 brain neurons as well as neurons in certain brain cell groups compared to control animals without co

149 later time points, PrP(Sc) was localized to brain cell groups that directly project to the hypogloss

150 ing effects of gonadal secretions, XY and XX brain cells have different patterns of gene expression t

151 ent of mitochondria in neurogenesis in human brain cells have not been well explored.

152 tosine methylation between spermatogenic and brain cells, identifying 223 new candidate tissue-specif

153 ruses can infect and replicate and spread in brain cells if not blocked by interferon-stimulated gene

154 In parallel work with cultured primary human brain cells, IFN and poly(I:C) treatment reduced hCMV in

155 Similar to the case with cultured brain cells, IFN treatment of the developing brain in vi

156 ble gliomas without evident damage to normal brain cells in all 24 mice assessed.

157 evaluation of the effects of oHSVs on normal brain cells in animal models is needed to enhance our un

158 TLR3 protein is present in brain cells in early embryonic stages of development, an

159 We also found that very few of these brain cells in male hybrids are in S phase, as determine

160 interplay of breast cancer cells and native brain cells in metastasis is poorly understood and rarel

161 um signaling tunes numbers of differentiated brain cells in regenerative growth and tissue remodeling

162 Brain cells in situ contain low concentrations of free p

163 Transduction of rat brain cells in situ with a lentiviral vector expressing

164 ect on the viability and plasticity of major brain cells in the presence or absence superparamagnetic

165 P expression in astrocyte and glial-enriched brain cells in vitro, suggesting that this pro-inflammat

166 ls and virally infected target Ag-presenting brain cells in vivo during an antiviral brain immune res

167 occurred in primary cell cultures, embryonic brain cells in vivo, and cells in healing skin wounds an

168 rotective through direct effects on ischemic brain cells, in addition to effects on inflammation.

169 led to quantifying populations of different brain cells, including myelin-forming oligodendrocytes.

170 the absence of both centrosomes and the SAC, brain cells, including neural stem cells, experience mas

171 insic preference for infection of developing brain cells, independent, but not mutually exclusive, of

172 Thus, upon infection, resident brain cells induced a breadth of innate immune responses

173 A genome, which replicates only in the first brain cell infected, as corroborated with ultrastructura

174 in mice leads to decreased life expectancy, brain cell injury, and hypersensitivity to interferon.

175 Ags released by neurocytotoxic Abs or other brain cell injury, and the resulting immune complexes st

176 mutations contribute functional diversity to brain cells is a long-standing question.

177 The intense osmotic stress sustained by brain cells is believed to be the major risk factor for

178 essed in brain tumor cells but not in normal brain cells is important for understanding the molecular

179 Transgenic manipulation of subsets of brain cells is increasingly used for studying behaviors

180 Deletion of SOCS-3 from brain cells is known to protect mice from diet-induced o

181 ow extensive methylation patterns vary among brain cells is unknown and bipolar methylated genomic lo

182 otein (apo) E4 is expressed in many types of brain cells, is associated with age-dependent decline of

183 ze vesicles and induce cytotoxicity in a rat brain cell line.

184 ta, albeit initially from only two cancerous brain cell lines for a limited number of epigenetic mark

185 ve inhibitor of ferrochelatase, in two human brain cell lines, SHSY5Y (neuroblastoma) and U373 (astro

186 ction of HIV regulatory proteins in infected brain cells may contribute to neurological damage.

187 toward efflux of specific proteins from the brain, cell-mediated immune responses, and other mechani

188 ways at both the blood-brain barrier and the brain cell membrane and undergoes both import from the b

189 ecognition site but also by an alteration of brain cell membrane structure secondary to conjugated di

190 Phospholipids in the brain cell membranes contain different polyunsaturated f

191 ochondrial dysfunction, methods for studying brain cell metabolism at high spatial resolution are nee

192 s that Mn transport into/distribution within brain cells mimics that of other biologically relevant m

193 etary (poly)phenols may cross the BBB, reach brain cells, modulate microglia-mediated inflammation an

194 previously shown that CMV infects developing brain cells more easily than it infects mature brain cel

195 inguishing and quantitatively characterizing brain cell morphologies noninvasively.

196 es to explore the possibility of quantifying brain cell morphology noninvasively.

197 The transfected brain cells near the injection site appeared to be mostl

198 be the generation of ketones, which provide brain cells (neurons and astrocytes) with an energy sour

199 These markers are not co-expressed in normal brain cells nor in tumorous brain cells.

200 Brain cells normally respond adaptively to bioenergetic

201 tric assay, based on the analysis of unfixed brain cell nuclei, to study whether p75(NTR)-dependent n

202 restored brain:body proportion by increasing brain cell number through epimorphosis or decreasing bra

203 ll number through epimorphosis or decreasing brain cell number through tissue remodeling (morphallaxi

204 due to the cellular changes in blood and/or brain cell number, activation state and their cytokine/g

205 lantation, we demonstrated that adult monkey brain cells, obtained from cortical biopsies and kept in

206 1) upon HIV-1 infection and its elevation in brain cells of AIDS patients with dementia.

207 tegration of human oncogenes into endogenous brain cells of immunocompetent mice.

208 e that the endoplasmic reticulum (ER) in the brain cells of these mice is structurally abnormal.

209 H2S3 and H2S were produced from 3 MP in the brain cells of wild-type mice but not 3MST knockout (3MS

210 tions were attributable to direct effects on brain cells or indirect effects mediated via peripheral

211 ute to pathogenesis by stimulating intrinsic brain cells or recruiting macrophages to the brain.

212 al to the control of motor activity, whereas brain cells other than forebrain neurons (likely glial c

213 he infected tumor cells, but not of infected brain cells outside the tumors.

214 explored, potentially fundamental aspects of brain cell physiology.

215 ime that PEGylated nanoparticles evade major brain cell populations - a phenomenon which will enhance

216 We identify the brain cell populations that are most susceptible to ZIKV

217 on-free, transient NIR photonic approach for brain cells possesses remarkable potential to add new di

218 We have previously shown that fetal rat brain cells, preneuronal (PC12), and hepatocyte (CWSV-1)

219 Investigations were performed with brain cell preparations obtained from 9 donors.

220 Chronic hyperglycemia also decreased brain cell proliferation in most neurogenic niches throu

221 ain psychotropic drug-induced actions on SVZ brain cell proliferation.

222 the TRalpha selective agonist CO23 increased brain cell proliferation; whereas, treatment with the TR

223 ulted from the methylation differences among brain cells rather than from asymmetric DNA methylation

224 microanatomy of immune clearance of infected brain cells remains poorly understood.

225 y-state level, with an impact on surrounding brain cells, remains unknown.

226 and the polyamines play an essential role in brain cell replication and differentiation and polyamine

227 and the polyamines play an essential role in brain cell replication and differentiation.

228 us, neural cell lines and heterogeneous, rat brain cells, respectively.

229 -ganglioside in the endoplasmic reticulum of brain cells results in calcium imbalance, induction of a

230 pend completely on an external supply (e.g., brain cells, roots and seeds).

231 lls differed in phenotype, indicating that a brain cell's complement of sex chromosomes may contribut

232 solution studies and an improved modeling of brain cell shapes and mechanical properties, could help

233 port that ATP levels, the energy currency of brain cells, show a surge in the initial hours of sponta

234 Discrete populations of brain cells signal heading direction, rather like a comp

235 vealed that contributions from nonneoplastic brain cells significantly influence the expression patte

236 antation system that allows control of fetal brain cell survival and differentiation by pre-assembly

237 These results indicate that NPD1 promotes brain cell survival via the induction of antiapoptotic a

238 this promotes the pain phenotype and, in the brain, cell survival or differentiation.

239 was in the range 3.0-4.1, and increased with brain cell swelling after water intoxication.

240 l ADC was reduced in both groups (indicating brain cell swelling).

241 tive disorders, if and how LTL is related to brain cell telomere shortening, and whether telomere sho

242 ML) is caused by the infection of particular brain cells, termed oligodendrocytes, by the JC virus.

243 t Al-Abeta42 would have more ready access to brain cells than Abeta42.

244 ectivity for killing GBM cells versus normal brain cells than VSV with wild-type M protein.

245 of NF-1 class D mRNA were expressed by human brain cells that are highly susceptible to JCV infection

246 brain, and that cause mosaics of monoallelic brain cells that differentially express wild-type and mu

247 activation and identified a critical pair of brain cells that induces the entire feeding sequence whe

248 persensitive (DH) sites within the PWS-IC in brain cells, then identified transcription factor bindin

249 exposure may interfere with the activity of brain cells, thereby generating behavioral and cognitive

250 OI analyses confirmed that the propensity of brain cells to accumulate excessive iron as a function o

251 HSF1 plays a crucial role in the response of brain cells to prenatal environmental insults and may be

252 nd interleukin-1 alpha (IL-1alpha) stimulate brain cells to yield increased levels of LG3.

253 CPF has been shown to inhibit replication of brain cells, to elicit alterations in neurotrophic signa

254 t targets predominantly neurons, <10% of the brain cells transduced with the RRV pseudotyped vector w

255 In a previous study on autologous brain cell transplantation, we demonstrated that adult m

256 We examined cultures for brain cell type and changes in cell type caused by exper

257 ctive infection in at least one normal mouse brain cell type.

258 ingle-nucleus methylomes expand the atlas of brain cell types and identify regulatory elements that d

259 We investigated which brain cell types express MLC1, compared developmental ex

260 However, isolated brain cell types have not been evaluated for either infe

261 zing detailed metabolic changes of different brain cell types in response to neurotoxins.

262 eplicates in and may be neurotoxic to normal brain cell types in vivo is poorly understood.

263 Metabolic specialization among major brain cell types is central to nervous system function a

264 Several brain cell types represent possible sources of NO.

265 lMapper makes accurate predictions for human brain cell types that have never been isolated, and can

266 d ABCA1 expression and function in different brain cell types using cultures of primary neurons, astr

267 ntal retardation protein (FMRP) in different brain cell types, especially in non-neuron glial cells,

268 iad of biological processes in virtually all brain cell types, including neurons.

269 s of allele-specific Ube3a expression in key brain cell types, thereby improving our understanding of

270 rge number of interactions between different brain cell types.

271 development has lagged behind that of other brain cell types.

272 les by all the major (immune and non-immune) brain cell types.

273 number of times and differentiate to normal brain cell types; whereas NBCs can divide an unlimited n

274 ng genes specifically expressed in different brain cell-types.

275 for a transgenic marker carried only by the brain cells, undifferentiated stem cells are recovered i

276 es that Abeta is not directly detrimental to brain cells until it reaches a threshold concentration.

277 en fluorescent protein-CIP (AAV9-GFP-CIP) to brain cells via intracerebroventricular infusion in amyl

278 Brain cells viability and plasticity were analyzed using

279 a indicated that neuronal PD-L1 signaling in brain cells was important for GBM patient survival.

280 The chromosomal repertoire of individual brain cells was then assessed by chromosome counting, sp

281 glucose (a glucose analog metabolized by all brain cells) was compared in rat and human brain tumors.

282 e the developmental potential of adult human brain cells, we applied conditions favoring the growth o

283 Using knock-out mice and primary brain cells, we connect a key pattern recognition recept

284 molecular mechanisms of Tat interaction with brain cells, we isolated a cDNA clone that encodes a nov

285 with rat astrocytes and glial-enriched mixed brain cells were also undertaken.

286 ixing with SY serum samples, suggesting that brain cells were elaborating labile inhibitory factors t

287 ng result was obtained: human frontal cortex brain cells were found to display "DNA content variation

288 Labeled brain cells were localized within known gustatory region

289 pernatant obtained from virus-infected fetal brain cells were measured simultaneously in microbead-ba

290 tly cross the blood brain barrier and target brain cells when applied to neurogenetic disorders such

291 lized predominantly in the nucleus of normal brain cells, whereas in primary brain tumors NRP/B was a

292 enuated the infection of all primary control brain cells, whereas most glioblastoma cell lines treate

293 The NEP was performed in microglial (MG) brain cells, which are highly sensitive for neuro-viral

294 erentiation of brain tumor cells from normal brain cells with a contrast signal ratio over 100.

295 e cells, we infected dissociated fetal human brain cells with adenoviruses bearing the gene for green

296 arrier (BTB) and targeting specific types of brain cells with drug release into the cell cytoplasm.

297 he presence of extra centrosomes, and larval brain cells with extra centrosomes can generate metastat

298 he development, differentiation, and loss of brain cells, with broad implications for the epilepsies

299 as the appearance of pathological tau inside brain cells, with cognitive impairments evident in virtu

300 r calcium is essential to the functioning of brain cells, yet the phenomenology and mechanisms involv