ライフサイエンスコーパス: EB

1 EB is primarily a disorder affecting the epithelial laye

2 EB is supported by the National Health and Medical Resea

3 EB levels in spinal cord parenchyma determined capillary

4 EB-NS can be uptaken by plants and remotely detected in

5 EB-NS fluoresce at 910 nm and the fluorescence intensity

6 EBs are essential for 480AnkG localization and stabiliza

7 se discussed in a talk presented at the 2019 EB/ASPET meeting, which was organized by Professor Joe B

8 To date, 60 deaths have occurred (28 EBd, 32 Bd).

9 ORR was 66% (EBd) vs 63% (Bd).

10 s in independent testing sets in DE: 0.6752, EB: 0.6156, and UKB: 0.5989; trained on EB and tested on

11 ecting the underlying molecular abnormality: EB simplex, junctional EB, dystrophic EB and Kindler EB.

12 of Brachyury-GFP was highly variable across EBs, while the spatial patterns as well as the dynamics

13 rowing MTs, but information about additional EB-binding zones on MTs has been limited.

14 read of synaptic inhibition between adjacent EB lamina.

15 Knockout mutants lacking all EBs are viable and fertile and display normal pulling fo

16 rinsic differentiation program common to all EBs is unknown.

17 AMPK(-/-) EBs exhibited reduced levels of Tfeb, a master transcrip

18 er, Met) were significantly reduced after an EB; that metabolites associated with skeletal muscle glu

19 tracking dynamic microtubule plus-ends in an EB-dependent manner or moving processively towards minus

20 Structural analyses revealed an EB-like +TIP-binding motif within the capsid major homol

21 In an updated analysis, EBd-treated patients homozygous for the high-affinity Fc

22 same core plasticity mechanisms as CO(2) and EB.

23 B and tested on UKB: 0.6133, DE: 0.5143, and EB: 0.6049.

24 We found that both AB and EB populations of DGCs recorded from epileptic rats rece

25 burns on >30% of total body surface area and EB.

26 ower than that at the O-R phase boundary and EB may serve as a rigorous quantitative measure of the d

27 neuron classes connecting the AOTU, BU, and EB represent discrete lineages, genetically and developm

28 ally distinct primordia of the AOTU, BU, and EB within the late larval brain.

29 initive subcompartments of the AOTU, BU, and EB.

30 ontrol) to 4.2, 6.6, and 7.76% in NB, MB and EB crumbs (fully gelatinized), respectively.

31 gs suggest that Dop1R1 signaling in E-PG and EB R2/4 m circuits are compared against each other, ther

32 Tau and EBs form a complex via the C-terminal region of EBs and

33 ts demonstrate that tau directly antagonizes EB function through a phosphorylation-dependent mechanis

34 DALv2 neurons form the anterior EB primordium, which starts out as a bilateral structure

35 m moves forward and merges with the anterior EB primordium.

36 As EBs differentiate into ECs, they become postmitotic, but

37 evelopment [4, 5], binds to the same site as EBs [6], and recent in vitro studies proposed DCX locali

38 potent chemotherapeutic agent [epothilone B (EB)] showed significantly lower systemic toxicity and hi

39 dy has evaluated the role of energy balance (EB) in modulating metabolic adaptation.

40 Endothelial barrier (EB) breaching is a frequent event during inflammation, a

41 polynomial and calculate the energy barrier (EB) for direct domain switching between two variants of

42 o this problem is to use an Empirical Bayes (EB) method that assumes the variances among genes follow

43 icantly attenuated the percentage of beating EBs in culture and expression of early and late myocardi

44 dministration of 17-beta-estradiol benzoate (EB) restored this escalated anxiety-like behavior in TTC

45 BERKO EBs expressed higher levels of key ectodermal and neural

46 A notable example is the exchange bias (EB) effect between an antiferromagnet or ferrimagnet and

47 y role in the transfer of the exchange bias (EB) effect from the FM/AF interface to the AF/pinned-FM

48 we report the control of the exchange bias (EB) in single-phase manganite thin films with nominallyu

49 on of Cep104 with CP110, Cep97, end-binding (EB) protein, and tubulin.

50 as a scaffold interacting with End-Binding (EB) proteins and membrane proteins such as Neurofascin-1

51 End-binding (EB) proteins associate with the growing tips of microtub

52 n GDP-tubulin and competes with end-binding (EB) proteins for binding to the microtubule plus end.

53 at MT plus ends and depends on end-binding (EB) proteins.

54 tions with plus-end microtubule tip-binding (EB) proteins.

55 lycopersicum L.) yield causing early blight (EB) disease in tropical environment.

56 howed increased extravasation of Evans Blue (EB) dye, and loss of endothelial cells and pericytes 1 d

57 jugating molecular vaccines with Evans blue (EB) into albumin-binding vaccines (AlbiVax), here we dev

58 yered pigment CaCuSi(4)O(10) (Egyptian Blue, EB) via ball milling and facile tip sonication into NIR

59 size- and shape-controlled embryoid bodies (EBs) and can be easily modified to control EB self-assem

60 that ERbeta was induced in embryoid bodies (EBs) and neural precursor cells (NPCs) during developmen

61 g during differentiation to embryoid bodies (EBs) and to fibroblast-like cells was driven by the huma

62 cells (VIM -/- ESCs) using embryoid bodies (EBs) formed from both cell types.

63 s of all germ layers within embryoid bodies (EBs) in a highly variable manner.

64 AS events observed in mouse embryoid bodies (EBs) undergoing a neuroectoderm-like state.

65 The ellipsoid body (EB) in the Drosophila brain is a central complex (CX) su

66 (AOTU) and bulb (BU) to the ellipsoid body (EB) of the central complex.

67 ridge gall (E-PG) neuron and ellipsoid body (EB) R2/R4m ring neuron circuits both negatively gate mot

68 on approximately 12 pairs of ellipsoid body (EB) R4 neurons to trigger the selection of nutritive sug

69 of these compartments is the ellipsoid body (EB), a structure formed largely by the axons of ring (R)

70 how that ring neurons of the ellipsoid body (EB-RNs) display spontaneous morning and evening neural a

71 ere, a live stem cell derived embryoid body (EB) based cardiac cell syncytium served as a biorecognit

72 roximately 43% of FACS-sorted embryoid body (EB) cells] from primed-state induced pluripotent stem ce

73 xpense of the endoderm during embryoid body (EB) formation.

74 e retrovirally birthdated either early-born [EB; postnatal day (P)7] or adult-born (AB; P60) DGCs.

75 col at rest or after an acute exercise bout (EB).

76 7 per mille (SD)), and human exhaled breath (EB; deltaD = -119.63 +/- 7.27 per mille (SD), delta(18)O

77 We collected endobronchial brush (EB) and bronchoalveolar lavage (BAL) samples from 39 ast

78 Epidermolysis bullosa (EB) is an inherited, heterogeneous group of rare genetic

79 Hereditary epidermolysis bullosa (EB) is associated with skin blistering and the developme

80 ce of each subtype of epidermolysis bullosa (EB) is essential before clinical trials can be designed

81 Epidermolysis bullosa (EB), a group of complex heritable blistering diseases, i

82 he heritable forms of epidermolysis bullosa (EB), a phenotypically heterogeneous group of skin fragil

83 in-blistering disease epidermolysis bullosa (EB), we show that large numbers of cells, often in exces

84 s, such as junctional epidermolysis bullosa (EB).

85 ctural plasticity induced by ethyl butyrate (EB) or carbon dioxide (CO(2)) closes within 48 h after e

86 Cell apoptosis was detected by EB/AO staining, and cell cycle was analyzed by flow cyto

87 h a greater induction of TPH 2, and 5-HTT by EB in DRN that play key roles in emotion regulation.

88 This bias is further enhanced by EBs and Lis1.

89 Both CD38(+) hPGCLCs and CD38(-) EB cells significantly expressed PRDM1 and TFAP2C, altho

90 (EBs) and can be easily modified to control EB self-assembly kinetics.

91 ups: complete resection achieved en-bloc (CR-EB), complete resection achieved non-en-bloc (CR-NEB), a

92 pathologic and treatment characteristics, CR-EB and CR-NEB margin status were found to be independent

93 redictors of improved OS (relative to IR, CR-EB hazard ratio [HR] 0.65, 95% confidence interval [CI]

94 The CR-EB cohort comprised 749 (76%) patients, CR-NEB 159 patie

95 was significantly higher in patients with CR-EB (28 mo, P = 0.01) and CR-NEB resections (24 mo, P = 0

96 lary ultrastructure, significantly decreased EB extravasation into spinal cord parenchyma, meaningful

97 arge-field neurons and that early developing EB neurons play an important regulatory role in EB lamin

98 cs spontaneously occurring within developing EBs.

99 lotuzumab with bortezomib and dexamethasone (EBd) or bortezomib and dexamethasone (Bd) until disease

100 EB, and 22.9% autosomal dominant dystrophic EB.

101 ality: EB simplex, junctional EB, dystrophic EB and Kindler EB.

102 B, 34.3% with autosomal recessive dystrophic EB, and 22.9% autosomal dominant dystrophic EB.

103 ared with patients with recessive dystrophic EB.

104 bulk Brillouin zone and 6 eV binding-energy (EB) interval was acquired in approximately 3 h thanks to

105 al differentiation of daughter enteroblasts (EBs).

106 lu) in restricting the fate of enteroblasts (EBs) in the Drosophila intestine.

107 testinal stem cells to produce enteroblasts (EBs) and enterocytes (ECs) that regenerate the gut.

108 ysis using the doxycycline-inducible Etv2 ES/EB system showed increased levels of cell cycle genes in

109 that the excitability of SLC5A11-expressing EB R4 neurons increases dramatically during starvation a

110 The role of native (NB) and extruded (EB) banana starch, and a 1:1 native:extruded banana star

111 he nuclear abundance of transcription factor EB (TFEB) and nuclear factor of activated T cells (NFAT)

112 ssion is upregulated by transcription factor EB (TFEB) and other members of the MiTF/TFE family of tr

113 ng gene expression, via transcription factor EB (TFEB) and other transcription factors.

114 factors (TFs), such as transcription factor EB (TFEB) and transcription factor E3 (TFE3), are emergi

115 mTOR complex 1 (mTORC1)-transcription factor EB (TFEB) axis in the host cells.

116 Transcription factor EB (TFEB) functions as a master controller of lysosomal

117 y overexpression of the transcription factor EB (TFEB) gene was effective in improving muscle patholo

118 Because transcription factor EB (TFEB) has recently emerged as a master regulator of

119 egradation and promoted transcription factor EB (TFEB) nuclear localization.

120 iptionally regulated by transcription factor EB (TFEB) through the induction of genes involved in lys

121 Recently, transcription factor EB (TFEB) was implicated in expression of autophagy and

122 More recently, transcription factor EB (TFEB), a major regulator of autophagy and lysosomal

123 Transcription factor EB (TFEB), a master regulator of autophagy and lysosome

124 s known to activate the transcription factor EB (TFEB), a master regulator of lipid metabolism and ly

125 Here we show that transcription factor EB (TFEB), a master regulator of lysosomal biogenesis an

126 ia dephosphorylation of transcription factor EB (TFEB), a master regulator of lysosomal biogenesis an

127 Transcription Factor EB (TFEB), a master regulator of lysosomal biogenesis an

128 cid export based on the transcription factor EB (TFEB), a master regulator of lysosomal biogenesis th

129 We report here that the transcription factor EB (TFEB), a master regulator of lysosomal biogenesis, p

130 es an activation of the transcription factor EB (TFEB), a master regulator of lysosomal functions and

131 e via Akt modulation of transcription factor EB (TFEB), a master regulator of lysosomal pathways.

132 criptional regulator of transcription factor EB (TFEB), a master transcription factor of lysosomal bi

133 by up-regulation of the transcription factor EB (TFEB), which was down-regulated in cystinosis.

134 Here we show that transcription factor EB (TFEB)-a master transcriptional regulator of lysosoma

135 ar translocation of the transcription factor EB (TFEB).

136 lysosomal genes through transcription factor EB (TFEB).

137 ar translocation of the transcription factor EB (TFEB).

138 uclear translocation of transcription factor EB (TFEB).

139 mycin activity, reduced transcription factor EB activity, and a lower lysosomal mass.

140 nucleus, ACSS2 binds to transcription factor EB and translocates to lysosomal and autophagy gene prom

141 ysosomal stress-sensing transcription factor EB and, eventually, cell death.

142 Consequently, the transcription factor EB enters the nucleus, and autophagy is up-regulated.

143 regulator of autophagy transcription factor EB or treatments with the autophagy enhancers rapamycin

144 n of the mTOR substrate transcription factor EB to the nucleus and activation of autophagy-related ge

145 uclear translocation of transcription factor EB, a known activator of lysosomal gene transcription.

146 key autophagy genes and transcription factor EB, a master regulator of lysosomal biogenesis.

147 and autophagy genes via transcription factor EB, which increased lysosomal biogenesis and activation

148 Transcriptional factor EB (TFEB) is a nutrient and stress-sensing transcription

149 Here we describe a more flexible EB method, capable of capturing a much wider range of di

150 y for BAL fluid samples and 80% accuracy for EB samples.

151 pluripotency markers decreased similarly for EBs of both cell types; however, VIM -/- EBs had impaire

152 cinoma-derived xenografts compared with free EB and non-BNPs loaded with EB.

153 ventually a cure for patients suffering from EB, a currently intractable disease.

154 Furthermore, EB-NS display no bleaching and high brightness compared

155 Here we investigate the mechanisms governing EB/tau interaction in cell-free systems and cellular mod

156 Cell transplantation of hiPSC-EB-HLC in a rat model of acute liver failure significant

157 The resultant hiPSC-EB-HLCs expressed liver-specific genes, secreted hepatic

158 The transplanted hiPSC-EB-HLCs secreted human albumin into the host plasma thro

159 arting from embryoid bodies of hiPSCs (hiPSC-EBs) for robust mass production of human hepatocyte-like

160 However, EB protein-dependent dynein plus end tracking was found

161 plasticity could be extended beyond 48 h if EB- or CO(2)-responsive olfactory sensory neurons (OSNs)

162 within tau microtubule-binding sites impairs EB/tau interaction and prevents the inhibitory effect of

163 ecially those from fragmented amylopectin in EB).

164 In summary, our study delineates findings in EB that have potential relevance for all chronic wounds,

165 in 16 distinct genes have been implicated in EB, encoding proteins influencing cellular integrity and

166 Fungal diversity was significantly lower in EB samples from patients with T2-high compared with T2-l

167 inheritance for a missense ITGB4 mutation in EB, thus expanding the mutational database and genotype-

168 Many in the field who have participated in EB research for many years were especially enthusiastic

169 neurons play an important regulatory role in EB laminae formation.

170 ccessions indicating their potential role in EB.

171 his study highlights a novel role for tau in EB regulation, which might be impaired in neurodegenerat

172 d median PFS of 22.3 months vs 9.8 months in EBd-treated patients homozygous for the low-affinity all

173 In EBs, hPGCLCs were identified exclusively in the outermos

174 Endoreplication occurs exclusively in EBs and newborn ECs that inherit EGFR and active MAPK fr

175 rmal lineage progression are synchronized in EBs.

176 with slower kinetics resulting in increased EB porosity and growth factor signaling.

177 uired and sufficient to drive damage-induced EB/EC growth.

178 gregation kinetics of EBs markedly influence EB structure, with slower kinetics resulting in increase

179 to LDpred that makes use of LD information, EB-PRS also achieved 37.9%, 33.6%, 8.6%, 36.2%, 40.6% an

180 revalence of each major subtype of inherited EB in the United States are now available that should as

181 ne the incidence and prevalence of inherited EB stratified by subtype in the United States during a 1

182 We find that tau inhibits EB tracking at microtubule ends.

183 We show that aggregation method instructs EB lineage bias, with faster aggregation promoting pluri

184 In this paper, we introduce EB-PRS, a novel method that leverages information for ef

185 ISC/EB-specific knockdown of the mitophagy-related genes Pin

186 rastructure and mitochondrial damage in ISCs/EBs.

187 , whereas a distinct 4E-BP1 phospho-isoform, EB-gamma, phosphorylated at Thr-70, Ser-83, and Ser-101,

188 ularly dominant in dystrophic and junctional EB.

189 olecular abnormality: EB simplex, junctional EB, dystrophic EB and Kindler EB.

190 hildren were recruited, 8.6% with junctional EB, 34.3% with simplex EB, 34.3% with autosomal recessiv

191 ex, junctional EB, dystrophic EB and Kindler EB.

192 nsity profiles of one of the three mammalian EB-proteins, EB3, fused with red fluorescent protein (RF

193 bends to adopt the ring shape of the mature EB.

194 no differences in overall liking between MB, EB and control, validating feasibility of including bana

195 the further investigation of the microtubule-EB-Cep104-tubulin-CP110-Cep97 network of proteins.

196 dicate that the structural MAP tau modulates EB subcellular localization in neurons.

197 sonication into NIR fluorescent nanosheets (EB-NS).

198 xtension of neuropil glia around the nascent EB and BU, and analyze the relationship of primary and s

199 al, Vienna, Austria, the network of national EB patient advocacy organizations.

200 on unrevealing possible mechanistic basis of EB resistance in wild tomato.

201 ular platform for the therapeutic control of EB response.

202 However, the molecular determinants of EB/tau interaction remain unknown, as is the effect of t

203 around the world working at the forefront of EB research.

204 ow that patients with the junctional form of EB have significantly more cells infiltrating their woun

205 and genotypic features of syndromic forms of EB to delineate the concept of syndromic versus nonsyndr

206 ocytes confirmed substantial infiltration of EB-affected skin with resting (CD45RA(+)) and activated

207 The molecular mechanisms of EB recovery are poorly understood.

208 n, have been involved in the pathogenesis of EB.

209 ns affecting the biomechanical properties of EB.

210 re formed by the extended binding regions of EB proteins.

211 The sign of EB depends on the magnitude of the cooling field.

212 The sign of EB is related to the frustration of antiferromagnetic co

213 The size of EB-NS can be tailored to diameters <20 nm and heights do

214 canum Peralta could be a potential source of EB resistance; however, its underlying molecular mechani

215 The study of EB has led to seminal advances in our understanding of c

216 The versatility of EB-NS is demonstrated by in-vivo single-particle trackin

217 is required for the specific accumulation of EBs in the proximal axon.

218 ary, depending on the combined activities of EBs and tau proteins.

219 Loss of Klu results in differentiation of EBs into EE cells.

220 calization to growing MT ends independent of EBs [7].

221 We also find that aggregation kinetics of EBs markedly influence EB structure, with slower kinetic

222 form a complex via the C-terminal region of EBs and the microtubule-binding sites of tau.

223 and prevents the inhibitory effect of tau on EB comets.

224 quired for the inhibitory activity of tau on EB localization to microtubule ends.

225 and UKB: 0.5989; trained on EB and tested on EB: 0.6565, DE: 0.5407, and UKB: 0.6043; trained on UKB

226 752, EB: 0.6156, and UKB: 0.5989; trained on EB and tested on EB: 0.6565, DE: 0.5407, and UKB: 0.6043

227 o showed significantly decreased parenchymal EB levels.

228 ic rate (RMR), is modulated by participants' EB status.

229 ponse or better occurred in 36% of patients (EBd) vs 27% (Bd).

230 near field responses and an unusual in-plane EB effect.

231 tructures are written with EBL on a positive EB-resist coated GaAs and developed followed by shallow

232 Klu is induced in Notch-positive EBs and its activity restricts cell fate towards the ent

233 he fan-shaped body primordium, the posterior EB primordium moves forward and merges with the anterior

234 e type II lineages DM1-4, form the posterior EB primordium.

235 Previously EB proteins have been shown to recognize a stabilizing G

236 dynamics and depend on end-binding proteins (EBs) [1].

237 Among them, end-binding proteins (EBs) accumulate at microtubule plus ends, whereas struct

238 End Binding proteins (EBs) recruit a diverse range of regulators of microtubul

239 eractors, particularly end-binding proteins (EBs), have emerged as potential key players in AIS forma

240 les in the presence of end binding proteins (EBs).

241 e adverse effect of diabetes on SCI, reduced EB dye extravasation, and limited the loss of endothelia

242 Further, M and E cells regulate EB-RNs via identified PPM3 dopaminergic neurons, which p

243 The 4D spectral function rho(EB; k) in the entire bulk Brillouin zone and 6 eV bindin

244 We finally show EB R2/R4m neurons are in contact with E-PG neurons that

245 ected by dystrophic, junctional, and simplex EB.

246 8.6% with junctional EB, 34.3% with simplex EB, 34.3% with autosomal recessive dystrophic EB, and 22

247 In summary, EB-NS have the potential for a wide range of bioimaging

248 e defects highlight the concept of syndromic EB.

249 bring these new tools to effectively tackle EB.

250 s interaction is dependent on the C-terminal EB homology region of EB1 and partially dependent on an

251 For example, transcription factor (TF)EB, which regulates autophagy and lysosome biogenesis, i

252 These results provide direct evidence that EB lamination is critical for local pre-synaptic inhibit

253 Using this model, we show that EB recovery requires a CD31 receptor-induced, robust gly

254 nson's disease and type 2 diabetes show that EB-PRS achieved 307.1%, 42.8%, 25.5%, 3.1%, 74.3% and 49

255 blocked GTP hydrolysis, we demonstrate that EBs bind with high affinity to the GTP conformation of m

256 The EB scheme thus unifies a body of observations on biologi

257 furcation with limited short-circuiting (the EB scheme).

258 ctron microscopy has recently identified the EB binding site as the interface of four tubulin dimers

259 A-A receptors to their axon terminals in the EB, and optogenetic stimulation coupled with electrophys

260 of the AF layer results in a control of the EB effect which has potential for device applications.

261 The primordium of the EB has a complex composition.

262 in the peripheral and central domains of the EB, respectively.

263 Majority of the EB-triggered metabolic changes were active from steroida

264 tion at the level of RMR is dependent on the EB status of the participants, being reduced to half aft

265 We find that the EB at the T-O phase boundary is lower than that at the O

266 We show here that the EB is sequentially innervated by small-field and large-f

267 3 dopaminergic neurons, which project to the EB and are normally co-active with EB-RNs.

268 control the recruitment of leukocytes to the EB-associated skin lesions.

269 Whether the EB binding region is identical to the GTP cap is unclear

270 t negative effect that cosegregates with the EB phenotype in an extended family.

271 stablish that the GTP cap coincides with the EB-binding region.

272 yers and the trophoblast was abnormal in the EBs of tetraploid ESCs compared with diploid ESCs.

273 Patch-clamp analysis indicates these EB neurons are highly sensitive to sleep loss, switching

274 Strikingly, the synaptic plasticity of these EB neurons is both necessary and sufficient for generati

275 rkers of synaptic strength, suggesting these EB neurons undergo "sleep-need"-dependent plasticity.

276 sion of cell division through its binding to EB-proteins.

277 , CXCR2(+), and CCR2(+) myeloid cells toward EB-derived blister fluids.

278 /rested, untrained/EB, and endurance trained/EB).

279 use data from UK and Estonian biobanks (UKB, EB) as well as case-control data from the German populat

280 heightened anxiety in TTC9A(-/-) mice under EB influence is consistent with a greater induction of T

281 /rested, endurance trained/rested, untrained/EB, and endurance trained/EB).

282 mutant promoters were rapidly silenced upon EB differentiation, indicating that transcription factor

283 Over seven days of differentiation VIM -/- EBs had altered morphology compared to WT EBs, with a ri

284 for EBs of both cell types; however, VIM -/- EBs had impaired differentiation towards the endothelial

285 was not significantly expressed in the whole EBs.

286 ct to the EB and are normally co-active with EB-RNs.

287 Participants were patients of all ages with EB.

288 gitudinal lattice compaction associated with EB protein binding and GTP hydrolysis.

289 ng the complete set of genes associated with EB revealed a heterozygous missense mutation in exon 5 o

290 Most children with EB exhibit signs of MGD.

291 tive ophthalmic examination of children with EB presenting over seventeen months including meibomian

292 e ocular surface evaluation in children with EB to include lid margin evaluation using a recognized c

293 ular surface anomalies seen in children with EB.

294 mpared with free EB and non-BNPs loaded with EB.

295 PFS was greater with EBd vs Bd (HR, 0.72; 70% confidence interval [CI], 0.59-

296 og-rank P = .09); median PFS was longer with EBd (9.7 months) vs Bd (6.9 months).

297 lly significant adverse events occurred with EBd vs Bd.

298 yrin-G (480AnkG) selectively associates with EBs via its specific tail domain and that this interacti

299 Furthermore, with EBs originating from patient's stem cells, this biosenso

300 /- EBs had altered morphology compared to WT EBs, with a rippled outer surface and a smaller size due