ライフサイエンスコーパス: EB

1 EB is supported by the National Health and Medical Resea

2 EB levels in spinal cord parenchyma determined capillary

3 EB proteins are viewed as central regulators of +TIPs an

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

5 EBs are essential for 480AnkG localization and stabiliza

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

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

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

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

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

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

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

13 read of synaptic inhibition between adjacent EB lamina.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 BERKO EBs expressed higher levels of key ectodermal and neural

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

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

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

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

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

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

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

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

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

49 ratio of Abs to denatured elementary bodies (EB) over live EB, recognized more synthetic MOMP peptide

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

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

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

53 n poorly differentiated TKO embryoid bodies (EBs) and teratomas.

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

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

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

57 omogeneous and synchronized embryoid bodies (EBs) of defined sizes from dissociated human induced plu

58 AR-gamma pathway in beating embryoid bodies (EBs) with defined media, we established an efficient ARV

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

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

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

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

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

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

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

66 insufficient determinants for embryoid body (EB) formation.

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

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

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

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

71 demyelinated axons inside ethidium bromide (EB) demyelination lesion in adult spinal cord.

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

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

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

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

76 Epidermolysis bullosa (EB) pruriginosa is a rare variant of dystrophic EB.

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

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

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

80 This bias is further enhanced by EBs and Lis1.

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

82 In CLASP-depleted cells, EBs localized along the MT lattice in addition to plus e

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

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

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

86 cs spontaneously occurring within developing EBs.

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

88 EB, and 22.9% autosomal dominant dystrophic EB.

89 pruriginosa is a rare variant of dystrophic EB.

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

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

92 in Notch activity in daughter enteroblasts (EB), and an increase in differentiated enteroendocrine (

93 fferentiated daughters, termed enteroblasts (EB).

94 al differentiation of daughter enteroblasts (EBs).

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

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

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

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

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

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

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

102 cal interaction between transcription factor EB (TFEB) and AR.

103 nuclear localization of transcription factor EB (TFEB) and expression of TFEB target genes.

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

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

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

107 ein-mediated control of transcription factor EB (TFEB) gene expression, TFEB nuclear translocation, a

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

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

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

111 utive activation of the transcription factor EB (TFEB) in RagA/B knockout mouse embryonic fibroblasts

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

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

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

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

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

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

118 ytoplasmic retention of transcription factor EB (TFEB), a major transcriptional regulator of the auto

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

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

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

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

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

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

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

126 tion in astrocytes with transcription factor EB (TFEB), a master regulator of lysosome biogenesis, wo

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

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

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

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

131 lysosomal genes through transcription factor EB (TFEB).

132 the lysosomal regulator transcription factor EB (TFEB).

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

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

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

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

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

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

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

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

141 n the activation of the transcription factor EB, a master regulator of lysosomal function and autopha

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

143 administration promotes transcription factor EB-mediated clearance of proteolipid aggregates that acc

144 phagosome formation and transcription factor EB-mediated lysosomal proteolysis.

145 ssion and activity of Transcriptional Factor EB (TFEB), which acts as a master regulator of autophagy

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

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

148 ch are aimed at developing new therapies for EB.

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

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

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

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

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

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

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

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

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

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

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

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

161 e platform for the production of homogeneous EBs from dissociated human pluripotent stem cells (hPSCs

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

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

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

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

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

167 ccessions indicating their potential role in EB.

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

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

170 In EBs, hPGCLCs were identified exclusively in the outermos

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

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

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

174 rmal lineage progression are synchronized in EBs.

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

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

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

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

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

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

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

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

185 rastructure and mitochondrial damage in ISCs/EBs.

186 ularly dominant in dystrophic and junctional EB.

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

188 o denatured elementary bodies (EB) over live EB, recognized more synthetic MOMP peptides and had high

189 e positive control group immunized with live EB and the fertility controls.

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

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

192 linker-associated proteins (CLASPs) modulate EB localization at MTs.

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

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

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

196 ring normal EB localization, whereas neither EB-CLASP interactions nor EB tail-binding proteins are i

197 n, whereas neither EB-CLASP interactions nor EB tail-binding proteins are involved.

198 of CLASP was sufficient for restoring normal EB localization, whereas neither EB-CLASP interactions n

199 This novel EB production technology may represent a versatile platf

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

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

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

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

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

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

206 ns affecting the biomechanical properties of EB.

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

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

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

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

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

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

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

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

215 determine exclusive plus-end localization of EBs in cells.

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

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

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

219 ability of polyaniline-based materials (PANI-EB and PANI-ES) was tested as a potential fining agent f

220 Finally, the capturing capacity of PANI-EB and PANI-ES against 4-EG was evaluated in a real wine

221 The analyses performed indicated that PANI-EB is more effective in removing 4-EG than PANI-ES, with

222 o showed significantly decreased parenchymal EB levels.

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

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

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

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

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

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

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

230 End-binding proteins (EBs) are master regulators of the +TIP complex; however,

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

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

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

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

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

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

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

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

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

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

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

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

243 t CLASPs facilitate GTP hydrolysis to reduce EB lattice binding.

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

245 influence the MT lattice itself to regulate EB and determine exclusive plus-end localization of EBs

246 aled that CLASP directly functions to remove EB from MTs.

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

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

249 ected by dystrophic, junctional, and simplex EB.

250 8.6% with junctional EB, 34.3% with simplex EB, 34.3% with autosomal recessive dystrophic EB, and 22

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

252 bring these new tools to effectively tackle EB.

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

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

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

256 aded into the microwells will compromise the EB formation process.

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

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 The primordium of the EB has a complex composition.

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

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

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

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

265 20 and 180 days post-AlloHCT showed that the EB-BSI density increased after aG-GVHD onset (0.95 infec

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

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

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

269 developmental germ layers, confirming their EB identity.

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

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

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

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

274 ene-expression and methylome analyses of TKO EBs revealed promoter hypermethylation and deregulation

275 predisposes pediatric AlloHCT recipients to EB-BSI.

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

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

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

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

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

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

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

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

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

285 +TIP complex; however, it is unknown whether EBs are regulated by other +TIPs.

286 was not significantly expressed in the whole EBs.

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