ライフサイエンスコーパス: body formation

1 ment of sacral and tail vertebrae (secondary body formation).

2 o the posterior skeleton and tail (secondary body formation).

3 the SN in PD and it is associated with Lewy body formation.

4 budding, and ESCRT-catalyzed multivesicular body formation.

5 RRK2-induced neuronal toxicity and inclusion body formation.

6 s involving vegetative swarming and fruiting body formation.

7 nd cheating behavior during asexual fruiting-body formation.

8 tion of UPS is not specific to PD or to Lewy body formation.

9 to ensure appropriate timing during fruiting body formation.

10 revents the switch and disrupts the embryoid body formation.

11 the efficient encapsidation and cytoplasmic body formation.

12 bition of translation or inhibition of the P body formation.

13 at includes swarming, predation and fruiting body formation.

14 , and the processes of primary and secondary body formation.

15 cell volume, DNA degradation, and apoptotic body formation.

16 single cell reversals, swarming and fruiting body formation.

17 ses and the therapeutic benefit of inclusion body formation.

18 required for directed motility and fruiting body formation.

19 s gliding motility for swarming and fruiting body formation.

20 ep-up in prey availability inhibits fruiting body formation.

21 rentiation capacity as indicated by embryoid body formation.

22 cogen leads to aberrant branching and Lafora body formation.

23 es about the mechanisms involved in fruiting body formation.

24 eta-d-allose-mediated inhibition of fruiting body formation.

25 events during the initial stages of fruiting body formation.

26 that reproduces the early stages of fruiting body formation.

27 al rates during the early stages of fruiting body formation.

28 ential for social (S-) motility and fruiting body formation.

29 ontraction, membrane blebbing, and apoptotic body formation.

30 levels persisted through 5 days of embryoid body formation.

31 the episodic nature of lunar crust or parent body formation.

32 meiotic sex chromosome inactivation, and XY body formation.

33 UBL domain of Dsk2 is critical for inclusion body formation.

34 yte infiltration, and eosinophilic inclusion body formation.

35 anslational repressors and facilitators of P body formation.

36 both SfaD and GpgA are required for fruiting body formation.

37 tional motility during swarming and fruiting body formation.

38 ns were defective in S-motility and fruiting body formation.

39 B permitted all events except ring and polar body formation.

40 for a short time before noticeable inclusion body formation.

41 inoic acid, or IFN-gamma induced PML-nuclear body formation.

42 including protein aggregation and inclusion body formation.

43 ring center, respectively, inhibiting polar body formation.

44 racellular VWF trafficking and Weibel-Palade body formation.

45 rane blebbing, cell shrinkage, and apoptotic body formation.

46 at includes vegetative swarming and fruiting-body formation.

47 n in ligase activity, thereby promoting Lewy body formation.

48 ation of ES cells in the absence of embryoid body formation.

49 he initiation of asexual and sexual fruiting body formation.

50 its motility during aggregation and fruiting body formation.

51 of misfolded proteins by promoting inclusion body formation.

52 d toxicity, lead accumulation, and inclusion body formation.

53 to other targets and may be linked to Heinz body formation.

54 disease, leads to a defect in Weibel--Palade body formation.

55 (shiitake mushroom) associated with fruiting-body formation.

56 al for both vegetative swarming and fruiting body formation.

57 e cycle that includes multicellular fruiting body formation.

58 developmental process of M. xanthus fruiting body formation.

59 ese strains rescued sporulation and fruiting body formation.

60 mation, cell surface blebbing, and apoptotic body formation.

61 terization of a mutant defective in fruiting body formation.

62 a complex life cycle that includes fruiting body formation.

63 d for developmental aggregation and fruiting body formation.

64 a complex life cycle that includes fruiting body formation.

65 promote PD pathogenesis by accelerating Lewy body formation.

66 ING finger and the B1 box, regulates nuclear body formation.

67 on of chemicals which restore their fruiting body formation.

68 ly from the presomitic mesoderm (PSM) during body formation.

69 mation, cell surface blebbing, and apoptotic body formation.

70 cuolization, DNA condensation, and apoptotic body formation.

71 e sensitive to Lfng dosage than is secondary body formation.

72 y to promote TTP expression and subsequent P-body formation.

73 overlapped with the changes during embryoid body formation.

74 mad signaling, as Smad3 deletion abrogated P-body formation.

75 al motility, predatory rippling and fruiting body formation.

76 ly expressed in the DCT, is critical for WNK body formation.

77 specific roles of family members in protein body formation.

78 est that the HSR does not mitigate inclusion body formation.

79 and Fas I expression during locust mushroom body formation.

80 formation, DNA fragmentation, and apoptotic body formation.

81 iral transcription occurs prior to inclusion body formation.

82 ion through to the terminal stage of Hassall body formation.

83 end of the dimer for paraspeckle subnuclear body formation.

84 also to investigate the biology of inclusion body formation.

85 m sorted single cells, and enhanced embryoid body formation.

86 egetative cells that contributed to fruiting body formation.

87 omosome inactivation (MSCI), and leads to XY body formation.

88 ordered assembly can play a role in nuclear body formation.

89 yclodextrin perturbed TRIM5alpha cytoplasmic body formation.

90 y results in an inherited disorder of ketone body formation.

91 5, which is essential for processing body (P-body) formation.

92 30-fold during the first 3 days of embryoid body formation, a culture system model of early embryoge

93 regation of misfolded proteins and inclusion body formation, a hallmark of neurodegenerative disease.

94 iparum, which results in reduced osmiophilic body formation, a marked decrease in female fitness, and

95 tility rates on hard and soft agar, fruiting body formation ability, and sporulation frequency during

96 on mutant exhibited a 24 h delay in fruiting body formation, accumulated less glycogen in the station

97 ve conditions is often hampered by inclusion-body formation after overexpression from T7 promoter-bas

98 h encode proteins that affect multivesicular body formation, also showed altered vacuolar morphology

99 LL-37 stimulates lipid body formation and activates cys-LT-synthesizing enzymes

100 ein overload in mutants that cause inclusion body formation and alpha1AT deficiency.

101 show strong defects in mRNA decapping and P body formation and are blocked in translational repressi

102 ced mono-ADP-ribosylation and subsequent Sec body formation and cell survival.

103 rable, the rate-limiting steps for inclusion body formation and death can be traced to different conf

104 in oxidation, haemoglobin instability, Heinz body formation and decreased erythrocyte lifespan.

105 Frz pathway, which is essential for fruiting body formation and differentiation.

106 sphorylation is required for heterochromatin body formation and DNA elimination, whereas it is dispen

107 (2+)](i), cell membrane integrity, apoptotic body formation and DNA fragmentation in cultured HepG2 c

108 Chemokine-induced lipid body formation and enhanced LTC(4) release were both med

109 from the cytoplasm to the membrane, fruiting body formation and EPS production were restored to the l

110 mily is critical for specification of caudal body formation and erythropoiesis.

111 ns and their assembly dynamics for new basal body formation and function are not well understood.

112 VPS4 ATPases function in multivesicular body formation and in HIV-1 budding.

113 ype seems to preclude lead-induced inclusion body formation and increases lead toxicity at the organ

114 ic traits, namely endoplasmic reticulum (ER) body formation and induction of indole glucosinolate (IG

115 ar basis and biological function of both sex body formation and meiotic sex chromosome inactivation (

116 complex is cytoplasmic and is involved in P-body formation and mRNA decay by promoting decapping.

117 at deadenylation is required for mammalian P-body formation and mRNA decay.

118 nal regulation of key regulators NAI1 for ER body formation and MYB51/122 for IGs biosynthesis).

119 ynuclein ubiquitination and its role in Lewy body formation and neurodegeneration remain poorly under

120 y tangles and senile plaques as well as Lewy body formation and nigral degeneration.

121 quitination may play a critical role in Lewy body formation and PD pathogenesis.

122 required for translational repression and P-body formation and plays an indirect role in mRNA decapp

123 ssion was necessary for TGF-beta-dependent P-body formation and promoted growth inhibition by TGF-bet

124 etion of fdgA resulted in defective fruiting body formation and reduced sporulation efficiency (1% th

125 n regulating mRNA degradation and processing body formation and reinforces the influence of phosphory

126 a complex life cycle which includes fruiting body formation and sporulation in response to starvation

127 n asgD null mutant was defective in fruiting body formation and sporulation on CF medium.

128 Defective fruiting-body formation and sporulation result from mutations in

129 ntification of a novel inhibitor of fruiting body formation and sporulation, beta-d-allose.

130 us, mrp, which is required for both fruiting body formation and sporulation.

131 is study that IgG or IL-5 also induces lipid body formation and subsequent leukotriene C4 production

132 stress and invasive bacterial pathogens in U body formation and suggest that this process contributes

133 s, and differentiation potential in embryoid body formation and teratoma assays.

134 scillatory Lfng during primary and secondary body formation and that posterior development is less se

135 nctions as a negative regulator for fruiting-body formation and that the proper level of Pkn2 is nece

136 importance of the Golgi network in lamellar body formation and the necessity of acidification of the

137 otent stem cells (hiPSC), bypassing embryoid body formation and the use of exogenous molecules, coati

138 tood, particularly the mechanisms triggering body formation and their role in nuclear function.

139 rmal and mesodermal lineages during embryoid body formation and under inductive conditions using reti

140 provide a molecular explanation for Balbiani body formation and, surprisingly, show that viable ferti

141 or Pat1p causes translational repression, P body formation, and arrests cell growth.

142 de endosome to Golgi traffic, multivesicular body formation, and autophagy.

143 pericellular and bridging fibrosis, Mallory body formation, and bile ductular reaction.

144 ion for the assembly of decapping factors, P-body formation, and constitutive decay of instable mRNAs

145 ring enveloped virus budding, multivesicular body formation, and cytokinesis.

146 d for Pdd1p phosphorylation, heterochromatin body formation, and DNA elimination.

147 f the pdu operon are required for polyhedral body formation, and immunoelectron microscopy shows that

148 ating its aggregation, fibrillogenesis, Lewy body formation, and neurotoxicity in vivo.

149 Organelle movement, Balbiani body formation, and oocyte fate determination are select

150 des co-ordinated group movement and fruiting body formation, and requires directed motility and contr

151 alize into basal bodies, thus blocking basal body formation, and the microtubule ribbon was completel

152 ever, the mechanisms that underlie inclusion body formation, and the precise relationship between inc

153 tered because of host codon usage, inclusion body formation, and the tight association of bacterial c

154 down, disappeared at the time of first polar body formation, and then reappeared as larger clusters i

155 nal accumulation of alpha-synuclein and Lewy body formation are characteristic to many neurodegenerat

156 data indicate that aggregation and inclusion body formation are mechanistically and temporally distin

157 piCCT1(r) also delays the onset of inclusion body formation as visualized via live imaging.

158 ique GlcCer species, and defects in lamellar body formation associated with decreased expression of t

159 amma-zeins could initiate and target protein body formation at specific regions of the rough endoplas

160 whereas VipD interferes with multivesicular body formation at the late endosome and endoplasmic reti

161 inhibition of infection was independent of P-body formation because expression of GFP-Dcp1a mutants t

162 thoracic and lumbar axial skeleton (primary body formation), but are largely dispensable for the dev

163 elf-organization is thought to drive nuclear body formation, but whether this occurs stochastically o

164 s in other species, suggesting that Balbiani body formation by amyloid-like assembly could be a conse

165 CDMP-1 in the notochord inhibited vertebral body formation by blocking migration of sclerotome cells

166 ies suggest that FL1 participates in protein body formation by facilitating the localization of 22-kD

167 g microtubules may be required for inclusion body formation by HtEx1 and that inclusion body formatio

168 , IbpA/B or ClpA does not suppress inclusion body formation by the aggregation-prone protein preS2-S'

169 ither Ca2+ or Sr2+ was required for fruiting-body formation by wild-type cells.

170 We demonstrate that macrophage lipid body formation can be induced by modified lipoproteins o

171 Thus, inclusion body formation can function as a coping response to toxi

172 ed whether-protein aggregation and inclusion body formation cause neurotoxicity are presently unknown

173 In mammalian testes, meiotic XY-body formation causes suppression of X-linked CstF-64 ex

174 rve as intermediates for fibrillar inclusion body formation, causes neurodegeneration.

175 and medium pH had little effect on inclusion body formation, co-overproduction of the dnaKJ operon, b

176 formation of the anterior skeleton (primary body formation), compared to the posterior skeleton and

177 virus, we showed that the onset of inclusion body formation corresponds to the onset of viral genome

178 cellular processes, including multivesicular body formation, cytokinesis, and viral budding, require

179 ribution of Buc in oocytes precedes Balbiani body formation, defining Buc as the earliest marker of o

180 Fruiting body formation depended on regulatory genes required ear

181 maH2AX with sites of DNA damage, reduced sex body formation, diminished Rad51 foci and absence of Mlh

182 Sec body formation does not depend on membrane traffic in th

183 We conclude that fruiting body formation does not occur exclusively in response to

184 plating method in which intervening embryoid body formation does not occur.

185 SigF is required for fruiting body formation during development as well as social moti

186 tive soil bacterium which undergoes fruiting body formation during starvation.

187 in vitro differentiation protocols (embryoid body formation, endodermal induction, directed different

188 ressed in M. xanthus, NafA restored fruiting body formation, EPS production, and S-motility to difA m

189 d for the hES-ATII cells, including lamellar body formation, expression of surfactant proteins A, B,

190 This progressive mode of body formation from the posterior end of the embryo requ

191 ncover a DNA under replication-53BP1 nuclear body formation-G1 arrest axis as an unanticipated outcom

192 r key factors proposed to be essential for P body formation, GW182, Edc3, and Edc4, were unaffected b

193 ondrogenesis by human ESCs required embryoid body formation; however, embryoid body formation often r

194 le to switch from slug migration to fruiting body formation i.e. unable to culminate.

195 rovides the first genetic access to Balbiani body formation in a vertebrate.

196 dependent on NAI1, a master regulator of ER body formation in Arabidopsis.

197 vels and structural modeling indicate that P-body formation in cells with the mutation in CCT3 is lin

198 Of importance, the defect of inclusion body formation in dsk2 mutants can be rescued by human u

199 Lipid body formation in eosinophils was a rapidly (<1 h) induc

200 ereas DeltagprADeltagprB eliminated fruiting body formation in homothallic conditions.

201 Moreover, it appears that lipid body formation in M. xanthus is an important initial ste

202 osphoproteins but play key roles in fruiting-body formation in M. xanthus.

203 se data uncover a new mechanism of apoptotic body formation in monocytes and also compounds that can

204 expression leading to multicellular fruiting body formation in Myxococcus xanthus.

205 y of using Zera technology to induce protein body formation in non-seed tissues.

206 required for translational repression and P-body formation in pat1Delta strains under these conditio

207 tor in vivo protein misfolding and inclusion body formation in real time.

208 memory predisposes the liver to Mallory Denk body formation in response to drug refeeding.

209 s of genes that are implicated in polyhedral body formation in Salmonella enterica.

210 among deadenylation, mRNP remodeling, and P-body formation in selective decay of mammalian mRNA.

211 nges are important contributors to inclusion body formation in several diseases.

212 sion, budded virus production, and occlusion body formation in SF-21 cells but not in TN-5B1-4 cells.

213 asgC767 and improved the quality of fruiting body formation in the asgB480 mutant.

214 r negatively controls multicellular fruiting body formation in the bacterium Myxococcus xanthus, inhi

215 es have demonstrated synuclein-positive Lewy body formation in the brains of individuals with parkins

216 ch as phosphorylation can regulate inclusion body formation in the context of alpha-synuclein and syn

217 causing mitotic abnormalities, 53BP1 nuclear body formation in the ensuing G1 phase, and G1 arrest.

218 We also demonstrate that basal body formation in the male testes and the production of

219 rexpression construct to restore prolamellar body formation in the porB-1 porC-1 double mutant backgr

220 f R6/2 HD mice and does not affect inclusion body formation in the R6/2 brain.

221 nd the developmental mechanisms of posterior body formation in the zebrafish, a fate map of the zebra

222 efficient late-gene expression and occlusion body formation in TN368 cells.

223 tiple hematopoietic lineages during embryoid body formation in vitro, but to date, an ES-derived hema

224 usion: SAMe treatment prevented Mallory Denk body formation in vivo and in vitro by preventing the ex

225 PML this motif is essential for PML nuclear body formation in vivo and PML-homo and hetero interacti

226 SAMe prevented Mallory Denk body formation in vivo.

227 ole in normal TE differentiation and Hassall body formation in vivo.

228 This treatment also inhibits spheroid body-formation in 3-dimensional culture.

229 dy, alone or coinjected, blocks second polar body formation, in vitro fertilization, or cytokinesis.

230 of beclin (a protein required for autophagic body formation) inhibited caspase-independent macrophage

231 dependently (0.01-100 nM) elicited new lipid body formation, intracellular LTC(4) formation at lipid

232 Whether inclusion body formation is an adaptive response or is directly re

233 Polar body formation is an essential step in forming haploid e

234 We determined that loss of Weibel-Palade body formation is associated with markedly reduced secre

235 Thus, an understanding of inclusion body formation is crucial for the discovery of innovativ

236 P-body formation is disrupted in A. nidulans strains delet

237 The findings provide evidence that inclusion-body formation is in itself a sufficient cause of neurod

238 levels are reduced, suggesting that primary body formation is more sensitive to Lfng dosage than is

239 es ciliogenesis, but the regulation of basal body formation is not fully understood.

240 When deadenylation is impaired, P-body formation is not restorable, even when mRNAs exit t

241 Though inclusion body formation is nuanced, it corresponds to a more gene

242 Moreover, P-body formation is reduced in strains lacking Sbp1p.

243 ld be further attributed to reduced lamellar body formation, loss of apical polarization of LB secret

244 We propose that the process of Lewy body formation may be akin to that of aggresome-like str

245 n body formation by HtEx1 and that inclusion body formation may have evolved as a cellular mechanism

246 nisms of and the factors regulating lamellar body formation must be better understood.

247 ere the meiotic apparatus attaches and polar body formation occurs following fertilization.

248 As in other organisms a dynamic shift in P-body formation occurs in response to diverse physiologic

249 Furthermore, inhibition of fruiting body formation occurs only when beta-d-allose is added t

250 ins and drives relocalization of HIRA to PML bodies, formation of SAHF and senescence, likely through

251 Fruiting body formation of Myxococcus xanthus requires the ordere

252 Fruiting body formation of Myxococcus xanthus, like biofilm forma

253 The prominent cytoplasmic body formation of TRIM5alpharh, which depended on the co

254 d embryoid body formation; however, embryoid body formation often results in heterogeneous differenti

255 and for cellular aggregation during fruiting body formation on starvation media.

256 ntingtin predicts whether and when inclusion body formation or death will occur.

257 ition occurred contemporaneously with parent body formation or shortly after it probably within 100 M

258 ls may not require yellow cells for fruiting body formation or starvation-induced sporulation of tan

259 growth, developmental aggregation, fruiting body formation, or sporulation.

260 and an upregulation of an alternative ketone-body formation pathway.

261 Although oil-body formation per se can occur independently of oleosin

262 Surprisingly, inclusion body formation predicts improved survival and leads to d

263 on the cell surface, is delayed in fruiting body formation, produces fewer spores, is delayed in ger

264 xploited to tackle the problems of inclusion body formation, proteolytic degradation and disulfide bo

265 extracellular signals required for fruiting body formation rather than in the sensing of such extrac

266 on of the cell cycle and impaired processing-body formation, reminiscent of Nanos2-knockout phenotype

267 nals that are known to induce and repress ER body formation, respectively.

268 This new site of polar body formation sets up a new animal-vegetal axis that or

269 During this process of fruiting body formation, short-range C-signaling between cells re

270 ts in high CO2 but not later steps (fruiting body formation, sporulation), indicating a major role fo

271 embryonic stem (hES) cells rely on embryoid body formation, stromal feeder co-culture or selective s

272 Data from embryoid body formation studies indicated that the Mp(-/-) EBs ha

273 odegenerative process in disorders with Lewy body formation, such as Parkinson's disease and dementia

274 In concert with increased P-body formation, TGF-beta induced expression of the ARE-b

275 inuous simulation all the stages of fruiting-body formation that have been experimentally observed: n

276 Pkn9 kinase activity caused altered fruiting-body formation, the absence of the KREP9 proteins in the

277 ull mutant had negligible effects on protein body formation, the betaRNAi and gammaRNAi alone only ca

278 EGG-5, we observe defects in meiosis, polar body formation, the block to polyspermy, F-actin dynamic

279 EBP gene nla4 affects the timing of fruiting body formation, the morphology of mature fruiting bodies

280 myofibrillar disorganization, with nemaline body formation, the pathological hallmark of NM.

281 the pfk-pkn4 operon did not inhibit fruiting body formation, the spore yield was low.

282 olonized D. discoideum spores after fruiting body formation; this observation, together with the abil

283 newly isolated mutants defective in fruiting body formation to determine a possible relationship betw

284 protein kinase (PKA) was found to control P body formation under all conditions examined.

285 in PKB activation, chemotaxis, and fruiting body formation upon nutrient deprivation.

286 ation has been reported to be required for P body formation, viral inhibition of deadenylation, throu

287 Inclusion body formation was consistent with an actin-dependent co

288 P-body formation was dependent on TGF-beta/Smad signaling,

289 Nuclear body formation was dependent upon a region of ETO N-term

290 No evidence of inclusion body formation was detected in the substantia nigra pars

291 U body formation was triggered by membrane damage in infec

292 -regulation of laforin cannot explain Lafora body formation, we conclude that malin functions to main

293 e precise role of calcium signaling in polar body formation, we used live-cell imaging coupled with t

294 lock in chromatin condensation and apoptotic body formation when nuclei from HeLa cells expressing la

295 Stress granule assembly is dependent on P-body formation, whereas P-body assembly is independent o

296 eric galectins are expressed during fruiting body formation which are 83% identical to each other in

297 results indicate that DCP5 is required for P-body formation, which likely facilitates efficient decap

298 ogenesis, S-motility, rippling, and fruiting body formation, while orfL is dispensable for these proc

299 t showed substantia nigra cell loss and Lewy body formation, with small numbers of cortical Lewy bodi

300 Embryoid body formation yielded beating cardiomyocyte-like cells,