ライフサイエンスコーパス: EB

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

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

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

4 al differentiation of daughter enteroblasts (EBs).

5 ccessions indicating their potential role in EB.

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

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

8 ular surface anomalies seen in children with EB.

9 bring these new tools to effectively tackle EB.

10 ns affecting the biomechanical properties of EB.

11 Participants were patients of all ages with EB.

12 EB, and 22.9% autosomal dominant dystrophic EB.

13 ch are aimed at developing new therapies for EB.

14 have low PPV for infections caused by 3GC-R EB.

15 ected by dystrophic, junctional, and simplex EB.

16 cteremias and 64 (0.7%) were caused by 3GC-R EB.

17 improved relative to ERalpha + oil and GFP + EB.

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

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

20 ularly dominant in dystrophic and junctional EB.

21 rmal lineage progression are synchronized in EBs.

22 cs spontaneously occurring within developing EBs.

23 ve been implicated in the pathophysiology of EBS.

24 rastructure and mitochondrial damage in ISCs/EBs.

25 was not significantly expressed in the whole EBs.

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

27 c injections of 17beta-estradiol-3-benzoate (EB, 10 mug) or oil vehicle.

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

29 8.6% with junctional EB, 34.3% with simplex EB, 34.3% with autosomal recessive dystrophic EB, and 22

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

31 a episodes caused by 3GC-R and 3GC-sensitive EB, 56% and 94%, respectively, were initially treated wi

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

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

34 Of 152 randomized patients (77 EBd, 75 Bd), 150 were treated (75 EBd, 75 Bd).

35 tients (77 EBd, 75 Bd), 150 were treated (75 EBd, 75 Bd).

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

37 -R EB, PPVs of prior colonization with 3GC-R EB (90-day window) and prior usage of cephalosporins or

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

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

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

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

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

43 The EBD accumulation in the heated tumors increased by nearl

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

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

46 Here, we describe AAV-PHP.eB and AAV-PHP.S, capsids that efficiently transduce the

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

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

49 nt for sepsis, prior colonization with 3GC-R EB and prior antibiotic use have low PPV for infections

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

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

52 This bias is further enhanced by EBs and Lis1.

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

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

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

56 broaden our knowledge about the mechanism of EBS and the neuromodulation of the human brain.

57 elationship between the circuitry engaged by EBS and the types of neural responses elicited by sensor

58 tert-butyl 3,4-epoxybutanoate (rac-(t)Bu 3,4-EB) and CO2 using bifunctional cobalt(III) salen catalys

59 EB treatment in the GFP (GFP + EB) and ERbeta (ERbeta + EB) groups failed to improve ep

60 FU enhanced delivery of both Evans blue dye (EBD) and Gadolinium-chelated N-(2-hydroxypropyl)methacry

61 Grade 1/2 infusion reaction rate was low (5% EBd) and mitigated with premedication.

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

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

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

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

66 scein amidite (FAM-ssDNA), ethidium bromide (EB), and graphene oxide (GO) are employed in the sensing

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

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

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

70 Similarly, ERalpha + EB animals exhibited enhanced NMDAR-mediated synaptic tr

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

72 EBs are essential for 480AnkG localization and stabiliza

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

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

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

76 the microtubule plus-end tracking proteins, EBs, at the proximal axon is decisive for AIS assembly a

77 or colonization and antibiotic use for 3GC-R EB bacteremia, and the consequences of guideline adheren

78 Of 9422 episodes, 773 (8.2%) were EB bacteremias and 64 (0.7%) were caused by 3GC-R EB.

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

80 Expression of the reporter construct EBS: beta-glucuronidase (GUS) was detected in Arabidopsi

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

82 The EBD binds to the suppressor ligand UDP-N-acetyl-beta-d-m

83 We calculated and compared EB-BSI densities in the following 3 subgroups: patients

84 that in patients who developed aG-GVHD, the EB-BSI density after onset of aG-GVHD would be higher th

85 20 and 180 days post-AlloHCT showed that the EB-BSI density increased after aG-GVHD onset (0.95 infec

86 ect of aG-GVHD onset on the first episode of EB-BSI using Cox proportional hazards models.

87 of enteric bacterial bloodstream infections (EB-BSI), this association has not been studied in humans

88 predisposes pediatric AlloHCT recipients to EB-BSI.

89 rd ratio of 1.47 (P = .077) on time to first EB-BSI.

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

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

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

93 nem monotherapy in patients with prior 3GC-R EB colonization and/or recent cephalosporin or fluoroqui

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

95 Electrical brain stimulation (EBS) complements neural measurements by probing the caus

96 The EBD crystallizes in a "closed" conformation, in contrast

97 s the prevalence of generalized intermediate EBS declined by 76.7% as a result of later subclassifica

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

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

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

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

102 EBM derived from EBs differentiated for 10 days with osteogenic media (+b

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

104 The crystal structure of the EBD dimer was solved to 2.2 A resolution.

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

106 The EBD does not bind to 1,6-anhydro-N-acetyl-beta-d-muramyl

107 in (3GC)-resistant Enterobacteriaceae (3GC-R EB), Dutch guidelines recommend beta-lactam and aminogly

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

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

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

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

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

113 Our findings explain both EBs end-tracking behavior and their effect on microtubul

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

115 Most children with EB exhibit signs of MGD.

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

117 We document that the EBD exists exclusively as a dimer, even at a concentrati

118 BERKO EBs expressed higher levels of key ectodermal and neural

119 g the plus-end tracking end-binding protein (EB) family.

120 ed by autoradiography, by histology, and for EBD fluorescence to assess BBB permeability.

121 = 0.004) in BBB permeability, as assessed by EBD fluorescence.

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

123 rs with predicted effector binding elements (EBEs) for AvrHah1.

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

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

126 The key requirement for the successful EB formation in addition to the non-cell-adhesive round-

127 iR-29b increases sharply after embyoid body (EB) formation, which causes Tet1 repression and reductio

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

129 insufficient determinants for embryoid body (EB) formation.

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

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

132 early differentiation program common to all EBs, further establishing them as an in vitro developmen

133 , Horvath D, Benfenati E, Muratov E, Wedebye EB, Grisoni F, Mangiatordi GF, Incisivo GM, Hong H, Ng H

134 on compared with the ERalpha + oil and GFP + EB groups.

135 t in the GFP (GFP + EB) and ERbeta (ERbeta + EB) groups failed to improve episodic spatial memory rel

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

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

138 the prevalence of EBS overall and localized EBS had increased considerably by 30.4% and 25.5%, respe

139 The primordium of the EB has a complex composition.

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

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

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

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

144 In EBs, hPGCLCs were identified exclusively in the outermos

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

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

147 measured neural responses and the effects of EBS in primary visual cortex in four patients implanted

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

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

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

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

152 cooperative relationship between 480AnkG and EBs induces the assembly of microtubule-AIS structures i

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

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

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

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

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

158 EB is supported by the National Health and Medical Resea

159 rinsic differentiation program common to all EBs is unknown.

160 This Drosophila model of EBS is valuable for the identification of pathways alter

161 Epidermolysis bullosa (EB) is a group of mechanobullous genodermatoses characte

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

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

164 Importance: Epidermolysis bullosa simplex (EBS) is a group of clinically and genetically diverse me

165 and perivascular markers such as Evans blue (EB), isolectin B4 (IB4) or laminin (LN) are used alongsi

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

167 read of synaptic inhibition between adjacent EB lamina.

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

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

170 EB levels in spinal cord parenchyma determined capillary

171 o showed significantly decreased parenchymal EB levels.

172 m of EBS resulted in widespread formation of EBS-like cytoplasmic keratin aggregates in epithelial an

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

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

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

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

177 sociated with late-onset muscular dystrophy (EBS-MD) is an autosomal recessive disorder resulting fro

178 f the rod domain dictates the development of EBS-MD.

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

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

181 sensing system contains FAM-ssDNA probes and EB molecules.

182 of EBS resulting from EXPH5 mutations to the EBS-mottled pigmentation subtype.

183 eratin network formation and collapse due to EBS mutations remain incompletely understood.

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

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

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

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

188 ila, we identify a subset of ellipsoid body (EB) neurons whose activation generates sleep drive.

189 osomes leading to TFEB (transcription factor EB) nuclear translocation and activation of autophagy.

190 f the GabR effector-binding/oligomerization (Eb/O) domain suggest that binding a monocarboxylic gamma

191 A comparison between the structures of the Eb/O-PLP-AFPA complex and Asp-AT-PLP-AFPA complex reveal

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

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

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

195 The effector-binding domain (EBD) of AmpR was purified to homogeneity.

196 Spatial memory was examined 48 h after EB/oil treatment.

197 effectors can drive plant transcription from EBEs on either strand and in both directions.

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

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

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

201 For example, in 2002, the prevalence of EBS overall and localized EBS had increased considerably

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

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

204 This EB phenotype was fully rescued by BAC or cDNA complement

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

206 For bacteremia caused by 3GC-R EB, PPVs of prior colonization with 3GC-R EB (90-day win

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

208 thway and that inhibition of Hh signaling in EBs prevented DSS-stimulated ISC proliferation.

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

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

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

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

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

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

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

216 otes rapid hydrolysis of GMPCPP suggest that EB proteins modulate structural transitions at growing M

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

218 the calponin-homology domain of end-binding (EB) proteins but cannot bind directly to microtubules.

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

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

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

222 Effector binding elements (EBEs) recognized by native TAL effectors in plants have

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

224 Many fundamental questions about EBS remain unanswered, including the spatial extent of c

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

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

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

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

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

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

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

232 ) mutant that causes the most severe form of EBS resulted in widespread formation of EBS-like cytopla

233 ty disorders, and we propose the addition of EBS resulting from EXPH5 mutations to the EBS-mottled pi

234 skin disorder epidermolysis bullosa simplex (EBS) results from dominant mutations in keratin 5 (K5) o

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

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

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

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

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

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

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

242 onsense mutation in EXPH5 responsible for an EBS subtype with mottled pigmentation.

243 ary changes in this rare autosomal recessive EBS subtype.

244 Ralpha that received EB treatment (ERalpha + EB), such that memory was improved relative to ERalpha +

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

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

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

248 with the activation of transcription factor EB (TFEB) and Nrf2 transcriptional factors.

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

250 hydrolase-coordinating transcription factor EB (TFEB) as novel regulator of the human MuRF1 promoter

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

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

253 d lysosomal biogenesis, transcription factor EB (TFEB) in pancreatic cancer cells.

254 (mTOR) or activation of transcription factor EB (TFEB) mimicked a starvation effect in fed cells.

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

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

257 the autophagy-relevant transcription factor EB (TFEB) to the nucleus specifically after lysosomal ca

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

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

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

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

262 on of its activity with transcription factor EB (TFEB), a master regulator of lysosomal biogenesis, a

263 stigated a role for the transcription factor EB (TFEB), a master regulator of lysosomal biogenesis, i

264 e efficacy of targeting transcription factor EB (TFEB), a master regulator of lysosomal pathways, to

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

266 viral gene transfer of transcription factor EB (TFEB), a master regulator of lysosome biogenesis in

267 d reduced activation of transcription factor EB (TFEB), a master regulator of the autophagy-lysosome

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

269 -NCs, expression of the transcription factor EB (TFEB), the master regulator of lysosomal genes, and

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

271 lysosomal genes through transcription factor EB (TFEB).

272 the lysosomal regulator transcription factor EB (TFEB).

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

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

275 y mutant keratins and for the development of EBS therapies.

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

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

278 Hh signaling acted in EBs to regulate the production of Upd2, which activated

279 ces Hedgehog (Hh) signaling in enteroblasts (EBs) to promote intestinal stem cell (ISC) proliferation

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

281 of 1 x 10(11) vector genomes (vg) of AAV-PHP.eB transduced 69% of cortical and 55% of striatal neuron

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

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

284 to animals expressing ERalpha that received EB treatment (ERalpha + EB), such that memory was improv

285 EB treatment in the GFP (GFP + EB) and ERbeta (ERbeta +

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

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

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

289 lly significant adverse events occurred with EBd vs Bd.

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

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

292 After PET scanning, Evans blue dye (EBD) was injected into animals, and cryosections of the

293 verall incidence and prevalence of inherited EB were 19.60 and 8.22 per 1 million live births, respec

294 Is but yielded few viable elementary bodies (EBs) when macrophages were infected at a moderate (10) o

295 u(H)GBE(+) immature progenitor enteroblasts (EBs), whereas EEs are generated from ISCs through a dist

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

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

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

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

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