ライフサイエンスコーパス: shape change

1 suggest a simple design rule for controlled shape change.

2 tin polymerization, platelet activation, and shape change.

3 which correspond to the protein's effective shape change.

4 lets, which mediate platelet aggregation and shape change.

5 pe change, which defines the onset of tissue shape change.

6 memory polymer to regulate the time of such shape change.

7 umbers in a bilayered epithelium can lead to shape change.

8 rkers and TH2 cytokines, and eotaxin-induced shape change.

9 actomyosin redistribution together with cell shape change.

10 tures for cell proliferation, migration, and shape change.

11 rnover and generating the force for filament shape change.

12 d, putatively, diseases associated with cell shape change.

13 ex vivo prostaglandin D2-mediated eosinophil shape change.

14 activate G protein 13 signaling for platelet shape change.

15 thological platelet activation and amplifies shape change.

16 udies how the cytoskeleton controls cellular shape change.

17 that regulate NF-kappaB in response to cell shape changes.

18 es based on their past shape despite dynamic shape changes.

19 ntractility is critical for tissues to adopt shape changes.

20 long "track" MTs, resulting in dramatic cell shape changes.

21 nce of myosin motor activity cell and tissue shape changes.

22 Tissue morphogenesis is orchestrated by cell shape changes.

23 cell divisions, cell rearrangements and cell shape changes.

24 ynamics of N-BAR proteins relate to membrane shape changes.

25 s of stabilization to result in irreversible shape changes.

26 uce a variety of tissue movements and tissue shape changes.

27 ng to a comprehensive model for actin-driven shape changes.

28 ns, as well as a variety of resulting tissue shape changes.

29 pal mechanistic features underlying cellular shape changes.

30 es tight spatiotemporal coordination of cell shape changes.

31 is cancelled by cell rearrangements and cell shape changes.

32 process driven by asymmetric epidermal cell shape changes.

33 ental steps power cell-autonomous epithelial shape changes(1-3), which suggests the existence of spec

34 riven locomotion but retain the soft-bodied, shape-changing ability to explore confined environments.

35 RS spectrum or do not consider the spectra's shape change across time.

36 g the FABD fully rescued morphogenesis, cell shape change, actin regulation, and viability, whereas k

37 vestigated how physiologically relevant cell shape changes affect subcellular organization, and conse

38 The results show that there is no obvious shape change after solidification.

39 which reproduced the experimentally observed shape changes after surgical and photochemical operation

40 addition to these cell rearrangements, cell shape changes also contribute to tissue deformation.

41 Such molecular shape changes alter intermolecular packing and thus affe

42 During development, coordinated cell shape changes alter tissue shape.

43 These membrane reservoirs facilitate cell shape change and buffer mechanical stress, but we do not

44 issue organization and the basis of all cell shape change and cell movement in development.

45 ation and with CXCL8 to stimulate neutrophil shape change and chemotaxis.

46 supporting cells was also more sensitive to shape change and inhibition of MST1/2 in chicken utricle

47 the time-dependent correlation between cell shape change and intracellular factors that may play a r

48 deletion of NAP-2 markedly reduced leukocyte shape change and intrathrombus migration.

49 on-dependent cellular processes such as cell shape change and migration.

50 n-based cell protrusion into persistent cell shape change and migration.

51 t to elongation at the growth zone, but cell shape change and rearrangement contribute as much as 40%

52 Independent of mew, Rac regulates cell shape change and rearrangement in the proximal gland, wh

53 large scale tissue deformations, cell level shape change and subcellular F-actin organization and by

54 a lesser extent, width are major drivers of shape change and that these traits are still relatively

55 mptions by visualizing the stages of nuclear shape change and the corresponding evolution of the cort

56 od-shaped cells were committed to subsequent shape change and to becoming sonication-resistant spores

57 1-K38A eliminated this dynamic mitochondrial shape change and, importantly, blocked GSIS.

58 as a new model system for understanding cell shape change and, putatively, diseases associated with c

59 que cytoskeletal morphology to achieve rapid shape changes and a remarkable hunting strategy.

60 recise orchestration of cell migration, cell shape changes and cell adhesion.

61 o in wild-type protoplasts generates similar shape changes and cell division.

62 During development, coordinated cell shape changes and cell divisions sculpt tissues.

63 iors have been extensively studied, how cell shape changes and cell divisions that occur concurrently

64 This requires dramatic cell shape changes and cell movements, powered by the contrac

65 ells by MK571 or probenecid resulted in cell shape changes and decreases in actin stress fibers and M

66 and Sox2), actomyosin disorganisation, cell shape changes and diminished resistance to neural fold r

67 Nuclear shape changes and HIV inhibition both mapped to the nucl

68 siderable interspecies variation in the cell shape changes and neighbor exchanges underlying appendag

69 In addition, gross cell shape changes and organelle movements buffer local Ca(2+

70 at focal adhesions in the regulation of cell shape changes and polarity.

71 sue morphogenesis requires control over cell shape changes and rearrangements.

72 isruption of tip links, leads to stereocilia shape changes and shortening.

73 ks driven by myosin activation controls cell shape changes and tissue morphogenesis during animal dev

74 ical mechanisms governing ligand-induced RNA shape-change and enables the development of cell-free an

75 sites and respond with filipodia protrusion, shape change, and surface area expansion to facilitate p

76 g of a hydrogel as the driving force for the shape change, and the temperature-dependent modulus of a

77 e result of coordinated cell movements, cell shape changes, and the organisation of pigment cells dur

78 nd heterogenous layouts that exhibit complex shape changes, and whose transformed shapes could be loc

79 hese classes of mechanical metamaterials for shape change applications like morphing structures.

80 While the mechanisms underlying this shape change are now well described, the functional impo

81 Shape changes are accompanied by a significant lowering

82 Although these cell shape changes are accompanied by an apparent large incre

83 Computer simulations indicate that micellar shape changes are associated with different binding of t

84 These cell shape changes are controlled by nonmuscle myosin II (NMI

85 Cell shape changes are determined by the interplay of cell wa

86 In vivo, many tissue-scale shape changes are driven by pulsatile contractions of in

87 Cell-shape changes are insured by a thin, dynamic, cortical l

88 Such shape changes are limited in mammalian ears, where suppo

89 sms that translate these signals into tissue shape changes are not well understood.

90 All the shape changes are reversible when the voltage is removed

91 These shape changes are shown to originate in the interplay be

92 Individual cell shape changes are the basis for the morphogenetic events

93 Cell shape changes are vital for many physiological processes

94 g cytokinesis, the cell undergoes a dramatic shape change as it divides into two daughter cells.

95 longevity pathways.Mitochondria can undergo shape changes as a result of fusion and fission events.

96 nding magnetocaloric cooling with reversible shape changes as high as 5.6% under only 1.3 T, or 3 T a

97 shape-change assay relative to the isolated shape change assay, potentially reflective of its relati

98 W039 retained its potency in the whole-blood shape-change assay relative to the isolated shape change

99 Cell-shape changes associated with processes like cytokinesis

100 and platelet aggregates stimulated leukocyte shape change at sites of endothelial injury; however, on

101 tors of innate immunity and undergo dramatic shape changes at all stages of their functional life cyc

102 Vertebrate embryos undergo dramatic shape changes at gastrulation that require locally produ

103 e, and uses lithium-ion insertion to produce shape changes at low voltages.

104 ion of molecular switches to stimulate rapid shape changes at the macroscale and thus to maximize act

105 raphy changes dramatically during neutrophil shape change (both locally and globally) and can be trig

106 , the materials not only exhibit substantial shape changes but also remember the functions in the ass

107 d inhibited PGD2-stimulated human eosinophil shape change, but importantly QAW039 retained its potenc

108 he mechanical feedback systems ensure robust shape changes, but if they go awry, they are poised to p

109 Endoderm cells move by amoeboid shape changes, but in contrast to other instances of amo

110 ical actin network controls many animal cell shape changes by locally modulating cortical tension.

111 duce functional changes in a device and that shape changes can be actuated via heating of printed com

112 Similar shape changes can be generated by contraction as well as

113 eloping zebrafish embryo as their successive shape changes can be visualized in real-time in vivo.

114 inuous case, we find that sufficiently large shape changes can drive reconfiguration on timescales co

115 its rheology sets the rate at which cellular shape changes can occur.

116 These features arise from the shape-changing capabilities of origami assemblies, which

117 develop through complex coordination of cell shape change, cell migration, and cell proliferation.

118 ables quantification of the dynamics of cell shape changes, cell interfaces and neighbor relations at

119 hormonal controls that orchestrate the cell shape changes, cell-cell junction remodeling and polariz

120 ithelial organ size and shape depend on cell shape changes, cell-matrix communication, and apical mem

121 enhanced chemoattractant-induced eosinophil shape change, chemotaxis, CD11b surface expression, and

122 of platelet biology, including aggregation, shape change, coagulation, and degranulation, as well as

123 Here we demonstrate a new reversible shape-changing component design concept enabled by 3D pr

124 Finally, we create several 2D and 3D shape changing components that demonstrate the role of k

125 port that MxA forms membraneless metastable (shape-changing) condensates in the cytoplasm consisting

126 ort that MxA formed membraneless metastable (shape-changing) condensates in the cytoplasm.

127 Locomotion is driven by shape changes coordinated by the nervous system through

128 Net cell shape change depends on whether cell shape is stabilized

129 and PIN1a suggests that PAN2-dependent cell shape changes do not involve any of these proteins, indi

130 l behaviors originate from the Fermi surface shape change due to pressure-induced band inversion.

131 host red cell undergoes an abrupt, dramatic shape change due to the sudden breakdown of the erythroc

132 ion furrow can also achieve the same type of shape change during cytokinesis without myosin contracti

133 l manner, this synctium undergoes remarkable shape change during development.

134 model was generated to simulate the nuclear shape change during differentiation and predict the forc

135 ce transducer that is essential for platelet shape change during hemostasis.

136 [7, 13], we find that over 74% of rapid eye-shape change during mammalian evolutionary history is di

137 Tjp1a is a novel regulator of cell shape changes during colour pattern formation and the fi

138 Cell shape changes during cytokinesis in eukaryotic cells hav

139 llular matrix (ECM) adhesions regulates cell shape changes during embryonic development and tissue ho

140 omyosin accumulation that drive initial cell shape changes during gastrulation.

141 We show that when body shape changes during growth, these models make opposing

142 ent that the cell nucleus undergoes dramatic shape changes during important cellular processes such a

143 tiate the regulation of NMII to mediate cell shape changes during MHB morphogenesis are not known.

144 Here, we have quantified shape changes during mouse heart looping, from 3D recons

145 ork beneath the cell membrane, to facilitate shape changes during processes like cytokinesis and moti

146 behavior, which may help accommodate tissue-shape changes during rapid developmental events.

147 ion and the ecological significance of brain shape changes during the evolutionary diversification of

148 Eukaryotic cells undergo shape changes during their division and growth.

149 We find that the specific sequence of cell-shape changes during VF formation is critically controll

150 s a powerful method to understand how tissue shape changes emerge from the complex choreography of co

151 n Shh(-/-) mutants, which recapitulate heart shape changes expected from a persistent dorsal mesocard

152 Platelets adherent to fibrin displayed shape change, exposure of procoagulant phospholipids, an

153 Here, we report shape changing films that are powered by DNA strand exch

154 egulate actin cortex remodeling and membrane-shape changes for cell polarization.

155 cular structure to achieve low-energy-driven shape changes for the first time.

156 e suppressive mutations lead to a major cell shape change, from the normal cylindrical shape to a bra

157 al lipid domains, often accompanied by their shape change, fusion or splitting.

158 Although conversion of light into shape changes has been reported and compared to artifici

159 FRD perturbations, whereas models with large shape changes have considerable FRD potential.

160 he physical basis for the regulation of cell shape changes, here, we use a cell-like system with a co

161 Shape-changing hydrogels that can bend, twist, or actuat

162 dependent, time-resolved information on cell shape changes (impedance) and dynamic mass redistributio

163 However, the role of mitochondrial shape change in cholestasis is not defined.

164 oskeleton to cell-cell junctions drives cell shape change in development and homeostasis.

165 Shape change in hydrogels has been induced by global cue

166 contributes to physiologically relevant cell shape change in intact organisms.

167 inding of Neph1 did not induce a significant shape change in Myo1c, indicating this as a spontaneous

168 al flow, drove a lamellipodial-to-filopodial shape change in suspended cells, and induced a novel act

169 clude by describing several forces likely to shape change in the medical liability environment over t

170 llular signals, signaling pathways, and cell shape changes in a noisy background.

171 elop a general mathematical model to examine shape changes in a permeable object subject to boundary

172 Cell shape changes in cytokinesis are driven by a cortical ri

173 d a small molecule, MF275, that also induced shape changes in Env.

174 a high-throughput image cytometer to assess shape changes in Escherichia coli during hyperosmotic sh

175 ynamics of these large-amplitude strains and shape changes in few-nanometre-scale particles.

176 g isoform M23-AQP4 (AQP4-OAP) triggered cell shape changes in glioma cells associated with alteration

177 ic tissues provides positional cues to drive shape changes in mammalian development during implantati

178 Shape changes in plant tissues affect the pattern of str

179 dent diversity of HIV-1 Envs as they undergo shape changes in proceeding down the entry pathway.

180 Responsive hydrogels that undergo controlled shape changes in response to a range of stimuli are of i

181 ning multiple domains that undergo different shape changes in response to different DNA sequences.

182 sts that these MyosinII meshworks drive cell shape changes in response to external forces, and thus t

183 /actin filament interactions underlying cell shape changes in response to guidance cues, plays a role

184 CPs) programmed to undergo three-dimensional shape changes in response to light are promising materia

185 stalline elastomers (LCE) undergo reversible shape changes in response to stimuli, which enables a wi

186 to encode a wide range of 3-dimensional (3D) shape changes in response to temperature.

187 In nonmammals, damage evokes shape changes in supporting cells, which can divide and

188 requently accompanied by protein-facilitated shape changes in the plasma membrane.

189 such interactions have been identified with shape changes in the sprouts and the associated rearrang

190 The macroscopic bidirectional shape changes in TMPAs could be correlated with changes

191 ctioning requires that cells undergo dynamic shape changes in vivo.

192 osin cortical contractility drives many cell shape changes including cytokinetic furrowing.

193 podocytes not susceptible to sema3a-induced shape changes, indicating that MICAL1 mediates sema3a-in

194 Localized cell shape change initiates epithelial folding, while neighbo

195 veness in vitro as measured by Ca(2+) -flux, shape change, integrin (CD11b) expression, and chemotaxi

196 ethods for quantitatively decomposing tissue shape changes into cellular contributions.

197 rradiation eventually results in undesirable shape changes, irradiation growth, that limit the servic

198 In a second step, the dynamic shape change is realized by cross-linking the P2VP domai

199 We find that shape change is regulated by a beta-catenin-mediated dec

200 apical cell surfaces, and the resulting cell shape change is thought to cause tissue folding.

201 rized; however, the mechanical basis of cell shape changes is largely unknown because of a lack of me

202 The extent of these shape changes is limited by the mechanical properties of

203 At the core of cell-shape changes is the ability of the cell's machinery to

204 ntractile systems coordinate to promote cell shape changes is unclear.

205 ated after vessel injury and undergo a major shape change known as disc to sphere transition.

206 (ECM), are known to drive cell branching and shape change largely through a myosin-II-mediated reorga

207 pical constriction is a widely utilized cell shape change linked to folding, bending and invagination

208 res strongly regulated by size, with axes of shape change linked to the actions of recently identifie

209 nd molecular motors is encapsulated within a shape-changing lipid vesicle.

210 structural systems that can achieve gigantic shape change, making them ideal as a platform for super

211 efit from this new kind of low-energy-driven shape-changing mechanism.

212 ercomes cortical tension to produce the cell shape changes needed for locomotion.

213 Specific cell shape changes occur at the point of deepest constriction

214 When these drastic shape changes occur rapidly, cell volume and surface are

215 Using a grid on its underside, the shape change of polymer sheet, as well as cell morpholog

216 the slow host-guest exchange and switchable shape change of the cavity, quantitative release and cap

217 how the method can be used to model nuclear shape changes of human-induced pluripotent stem cells re

218 r and mechanical processes that underlie the shape changes of individual cells and their collective b

219 t is transformed into units of strain by the shape changes of individual switches, until a threshold

220 g, but the interplay of these processes with shape changes of the material remains to be explored.

221 Dynamic shape changes of the plasma membrane are fundamental to

222 l is generally achieved by head movements or shape changes of the sound-emitting mouth or nose.

223 from alveolar type I and type II cells, cell shape changes of type I cells and migration of myofibrob

224 The shape-change of 3D printed smart materials adds an activ

225 e quantitatively account for this wing-blade shape change on the basis of cell divisions, cell rearra

226 anching clades but thermal performance curve shape changes on shorter time scales.

227 With shape changes once considered only possible with high en

228 ing, as well as other processes that require shape change or force generation.

229 her elongation mechanisms, specifically cell shape change, orientated cell division and cell rearrang

230 Moreover, quantitative analysis of filament shape change over time revealed that myosin XI generates

231 s to quantify tissue deformation and surface shape changes over the course of leaf development, appli

232 lding allows bleb inflation and dynamic cell-shape changes performed by migrating cells.

233 photopatterning, and iii) there is permanent shape change post-irradiation.

234 ingression during cytokinesis, a model cell-shape-change process.

235 orally controlled leukocyte adhesiveness and shape-changes promoting leukocyte attachment to the inne

236 0.46, P = .001) and end-expiratory tracheal shape change (r(s) = 0.40, P = .01).

237 Riboswitches are shape-changing regulatory RNAs that bind chemicals and r

238 Soft materials capable of programmable shape change require localized control of the magnitude

239 Dynamical cell shape changes require a highly sensitive cellular system

240 at the base of fissures fail to undergo cell shape changes required for fissure initiation.

241 plays an important role in the turgor-driven shape changes required for stomatal pore opening to occu

242 nd somatic control to enable next-generation shape changing robots are also discussed.

243 Specific shape changing scenarios, e.g., based on bending, or twi

244 self-fold to specified shapes in controlled shape changing sequences.

245 he electrical resistivity measurement with V shape change signals the transition from a Rashba type t

246 platform for super light-weight structures, shape-changing soft robots, morphing antenna and RF devi

247 oxLDL, but not native LDL, induced shape change, spreading, and phosphorylation of MLC (ser

248 ous microarchitectures designed for specific shape change strategies, e.g. sequential shape recovery.

249 Cell shape changes such as cytokinesis are driven by the acto

250 the membrane components as well as dramatic shape changes such as endocytosis, vesicular trafficking

251 orce imbalance at cell contacts induces cell shape changes, such as apical constriction or polarized

252 al epithelia, including epithelia undergoing shape changes, such as the fin folds.

253 Inherent adaptability should allow such shape-changing systems to measure numerous different env

254 sterior zonules may have a greater impact on shape change than the equatorial zonule and that choice

255 Apical constriction is a cell shape change that promotes epithelial bending.

256 Apical constriction is a cell shape change that promotes tissue remodeling in a variet

257 VF formation along the same sequence of cell-shape change that we observed in the actual embryo, with

258 ch flexible E153-R210 links mediate capsomer shape changes that control where pentons are placed to c

259 astrulation pathway triggers epithelial cell shape changes that drive gastrulation and tissue folding

260 cytoskeleton is a major determinant of cell-shape changes that drive the formation of complex tissue

261 skeleton within individual cells drives cell shape changes that fold tissues.

262 ntial to driving the cell movements and cell shape changes that generate tissue structure.

263 Morphogenesis is driven by small cell shape changes that modulate tissue organization.

264 n must be maintained during the complex cell shape changes that occur during cytokinesis in vertebrat

265 e role of NMIIA and NMIIB in regulating cell shape changes that occur during MHB morphogenesis.

266 even more regulatory events driving the cell shape changes that produce tubes of specific dimensions.

267 folding/unfolding can contribute to the cell-shape changes that promote embryonic morphogenesis.

268 is stimulus, rather than causing a temporary shape change, the CAN structure responds by permanently

269 both a-cells and alpha-cells and their cell shape changes, the extracellular diffusion of mating phe

270 er (LCE) matrix that can achieve macroscopic shape change through a liquid crystal phase transition.

271 cAMP)-dependent signaling modulates platelet shape change through unknown mechanisms.

272 ation of cell contractility coordinates cell shape change to construct tissue architecture and ultima

273 tress and displacement fields with simulated shape changes to accommodation in living lenses.

274 cently developed methods for relating tissue shape changes to cell dynamics have not yet been widely

275 apices, undergo a series of coordinated cell-shape changes to form a ventral furrow (VF) and are subs

276 broader cortical areas induces proportional shape changes to growth domains, demonstrating that both

277 zation, we demonstrate how to exploit subtle shape changes to infer cell wall material properties.

278 need to coordinate spindle positioning with shape changes to maintain cell-cell adhesion.

279 tion profiles drive the rapid and reversible shape change under actuation magnetic fields.

280 cuss how different types of local and global shape changes underlie distinct migration modes.

281 ly lower than those of existing submolecular shape-changing units.

282 ) have the ability to show large recoverable shape changes upon temperature, stress or magnetic field

283 lates between two defect configurations, and shape-changing vesicles with streaming filopodia-like pr

284 al cell junctions promotes robust epithelial shape changes via ratcheting.

285 )-mediated inhibition of thrombin-stimulated shape change was accompanied by diminished phosphorylati

286 domains into the hydrogels, light-activated shape change was achieved, while domains bearing magneti

287 The mechanical nature of this shape change was confirmed by polyhedrocyte formation fr

288 The degree of platelet spreading and shape change was quantified by confocal microscopy.

289 on, but neither additional eyespots nor wing shape changes were observed in forewings as expected of

290 onally modelling Ca(2+) release, endothelial shape changes were shown to alter the geometry of the Ca

291 it slightly enlarged meshwork faces and some shape changes, whereas LB1-deficient nuclei exhibit prim

292 entry into HeLa cells resulted in host cell shape changes, whereas the tarP mutant did not.

293 (AC) is a widely utilized mechanism of cell shape change whereby epithelial cells transform from a c

294 tural basis for the known dramatic molecular shape change, whereby the molecular length can increase

295 d nanoparticles initiates a rapid isothermal shape change which triggers the activation of multiple f

296 LPC component has higher influence on wafer shape change, which can reduce device yields.

297 nsition from reversible to irreversible cell shape change, which defines the onset of tissue shape ch

298 cochemical properties but also their dynamic shape changes, which are required in various essential f

299 rial architectures that exhibit programmable shape changes with temperature and time.

300 s, as they undergo large reversible uniaxial shape changes, with strains of 20-500% and stresses of 1