ライフサイエンスコーパス: cable

1 d by constricting a supracellular actomyosin cable.

2 s not change the regions of alternans in the cable.

3 luding a resistive strain gauge and an ionic cable.

4 tions by continual polymerization of F-actin cables.

5 locations using optical fibres or microwave cables.

6 associated with cortical longitudinal actin cables.

7 hat the junctional regions act like inverted cables.

8 cargos along F-actin bundles known as actin cables.

9 clumps, meshworks or double rings, and stars/cables.

10 cribed state on selectively stabilized actin cables.

11 s-linking parameters generates thicker actin cables.

12 he spatial and dynamical properties of actin cables.

13 risome protein in the stabilization of actin cables.

14 egates most organelles along polarized actin cables.

15 filaments forming long and flexible filament cables.

16 (i) It produced thicker, more pronounced HA cables.

17 o the dissociation of Gic1 from the filament cables.

18 Dia1) was identified as a generator of these cables.

19 rebellar Golgi interneurons acted as passive cables.

20 concrete cylindrical columns by spiral steel cables.

21 haracterized by externalization of conductor cables.

22 broadcasted through a medium such as air or cables.

23 for the contractile ring and possibly actin cables.

24 principles of optical guiding by fibre optic cables.

25 with bundles of parallel filaments in actin cables.

26 ach the nucleus to retrogradely moving actin cables.

27 ber cells accumulated disoriented transverse cables.

28 and this decrease is dependent on the actin cables.

29 e of the platform for constructing molecular cables, 1,3,5-trifluorenylcyclohexane (TFC) and its difl

30 the formation of the leading edge actomyosin cable, a structure that is essential for wound closure.

31 esults in long, bent, and hyper-stable actin cables, accompanied by defects in secretory vesicle traf

32 earing, MII-contractility-dependent node-and-cable actin network in the cell body cortex.

33 lays misoriented and architecturally altered cables, along with impaired secretory vesicle traffic.

34 Cable analysis of the neurons indicated that the axonal

35 an independent contractile unit, with actin cables anchored end-on to cadherin complexes at tricellu

36 configuration, aligned with the apical actin cable and adherens-junctions within chick and mouse neur

37 ic percussive test values (PTVs) measured by cabled and wireless electronic percussive testing (EPT)

38 of Gin4 or Shs1 results in the loss of actin cables and cell death, similar to the loss of Bnr1.

39 nnect to follower cells via peripheral actin cables and discontinuous adherens junctions, and lead mi

40 n-promoting factor (NPF) Bud6 generate actin cables and mediate polarized cell growth.

41 ions between the cortical longitudinal actin cables and plasma membrane in the shank region of growin

42 Bnr1 are required for the assembly of actin cables and polarized cell growth.

43 support were evaluated while walking without cables and reacting to the perturbations.

44 l to retract, a disrupted leading edge actin cable, and reduced zippering as leading edges meet, clos

45 protrusions and/or a contractile actomyosin cable, and these actin structures drive wound closure.

46 s localizations to cytoplasmic puncta, actin cables, and the contractile ring.

47 s: endocytic actin patches, polarizing actin cables, and the cytokinetic contractile ring.

48 d into large bundles of fibrils, or collagen cables, and the number of these cables (but not their si

49 tial for Bud14 functions in regulating actin cable architecture and function in vivo.

50 ism is critical for maintaining proper actin cable architecture, dynamics, and function.

51 in myosin V (myo52 myo51) null cells, actin cables are curled, bundled, and fail to extend into the

52 Actin cables are dynamic structures regulated by assembly, sta

53 In a yeast cell undergoing budding, cables are in constant dynamic turnover yet some cables

54 Actin cables are linear cytoskeletal structures that serve as

55 ost from cell extremities, actin patches and cables are reorganized into actin bodies, which are stab

56 er in a single assembly, termed as molecular cable, are promising next-generation materials for effec

57 A supracellular actomyosin cable around the wound coordinates cellular movements an

58 for the efficient assembly of an actomyosin cable around the wound, and constitutively active myosin

59 ed current source density of one-dimensional cables as well as morphologically realistic neurons and

60 junctions, where filamentous actin (F-actin) cables assemble.

61 ision site and directed transport of F-actin cables assembled elsewhere can contribute to ring assemb

62 the basis for comprehensive understanding of cable assembly and regulation.

63 tes actin filament binding to regulate actin cable assembly and stability in cells.

64 Proper cable assembly further requires Bud6.

65 ey target for cell cycle regulation of actin cable assembly in budding yeast, and suggests an underly

66 kinase 1 activity also was found to regulate cable assembly in vivo.

67 ivity is critical for normal levels of actin cable assembly in vivo.

68 fimbrin is a critical Cdk1 target for actin cable assembly regulation in budding yeast.

69 metaphase cells preferentially promote actin cable assembly through cyclin-dependent kinase 1 (Cdk1)

70 mitotic cyclin Clb2 were competent for actin cable assembly, and cyclin-dependent kinase 1 activity w

71 nsights into mechanisms for regulating actin cable assembly, we reconstituted the assembly process in

72 from the wound edge and defective actomyosin cable assembly.

73 iderm, proliferation, or supracellular actin cable assembly.

74 unction is required for proper Bni1-mediated cable assembly.

75 When nurse cells contract, actin cables associate laterally with the nuclei, in some case

76 ikely driven by contraction of an actomyosin cable at the boundary between the amnion and serosa.

77 ng contraction of a pluricellular actomyosin cable at the free edge.

78 ite the presence of a contractile actomyosin cable at the periphery of the wound.

79 AJs promotes the assembly of an actin-myosin cable at the wound margin; contraction of the actin cabl

80 ia rapidly assemble a contractile actomyosin cable at their leading edge, as well as dynamic filopodi

81 central element is composed of two parallel cables at a distance of approximately 100 nm, which are

82 As cable bacteria are present in many seasonally hypoxic sy

83 mmer, when bottom water hypoxia develops and cable bacteria are undetectable, the phosphorus associat

84 Cable bacteria dominate the sediment geochemistry in win

85 The specific electrogenic metabolism of cable bacteria generates a large buffer of sedimentary i

86 at the long-range electrogenic metabolism of cable bacteria leads to a dissolution of iron sulfides i

87 erlands), which suggest that the activity of cable bacteria, a recently discovered group of sulfur-ox

88 ion of iron-oxide-bound phosphorus driven by cable bacteria, as observed in this study, contributes t

89 and specifically the population dynamics of cable bacteria, can also induce strong seasonality in se

90 ggregates are cleared from the bud via actin cable-based retrograde transport toward the mother and t

91 cases inducing nuclear turning so that actin cables become partially wound around the nuclei.

92 A167E actin caused more dynamic actin cable behavior in vivo than observed with WT actin.

93 se matrices do not resemble the rope-like HA cables but occur in distinct sheets or rafts that can ca

94 of inhibition does not alter actin levels in cables but, instead, cable shape and functionality.

95 or collagen cables, and the number of these cables (but not their size) increases in desmin knockout

96 cables enhanced leukocyte adhesion to these cables, but it also had several unexpected effects.

97 hibition of F-actin or laser ablation of the cable causes neural fold separation.

98 Actin cables, composed of actin filament bundles nucleated by

99 Loss of these cables compromises orderly apical targeting of vesicles.

100 h the fish surface, and an extended parylene cable connected the underwater chest electrodes with the

101 and parallel phases with straight or curved cables, consistent with observations of cells overexpres

102 , the mechanical coupling between actomyosin cable contraction and cell crawling acts as a large-scal

103 ing force generated by a tissue-level myosin cable contributes to SG invagination.

104 ses the question: how is the length of these cables controlled?

105 lled out with dendrites and axons optimizing cable costs and conduction time while keeping the connec

106 In contrast, control cable deletions caused kinase-on output, whereas inserti

107 After cable disassembly induced by transient exposure to latru

108 usly unappreciated ATP requirement for actin cable disassembly.

109 Compromising formation of the cables does not prevent secretion, but results in disorg

110 A cable-driven robot was used to train nine patients with

111 ibit aberrant equatorial clustering of actin cables during ring assembly and are particularly suscept

112 Axons act like cables, electrically wiring the nervous system.

113 The two parallel cable elements form twisted helical structures that are

114 s distance over bundles of specialized actin cables emanating from the apical plasma membrane.

115 on of printed circuit boards and copper-core cables emitted large amounts of OM with Br-rich inclusio

116 ches we unveil the presence of an actomyosin cable encircling TEMs.

117 d an external one by the supracellular actin cables encircling the amnioserosa.

118 Here, we first derive a full cable energy function for cortical axons based on classi

119 y (HH) neuronal equations and then apply the cable energy function to precisely estimate the energy c

120 redicted, the addition of heavy chains to HA cables enhanced leukocyte adhesion to these cables, but

121 PT device were significantly higher than the cabled EPT device (P <0.05), indicating lower implant st

122 reless EPT device gives PTVs higher than the cabled EPT device, indicating lower implant stability, a

123 llagen fibrils are nanostructured biological cables essential to the structural integrity of many of

124 For long cables excitations occurs due to ectopic foci that occur

125 as they are actively transported along actin cables, Exo70p displays actin-independent localization t

126 lope via a Myo52 motor domain restores actin cable extension and retrograde flow in myoV mutants.

127 a lead exhibits time-dependent high rates of cable externalization exceeding 20% at >5 years of dwell

128 Cable externalization was found to be more common in the

129 edictors of electrical lead failure included cable externalization, higher left ventricular ejection

130 rs away if engagement of MyoE(MYO5) to actin cables fails.

131 ure (30%), battery failure (19%), or patient cable failure (14%), whereas only 13% were because of pu

132 The seal was a two-dimensional cable filled with saline and bounded on one side by memb

133 rlies the degree of compensation for passive cable filtering during propagation of EPSPs in dendrites

134 This movement, retrograde actin cable flow (RACF), is similar to retrograde actin flow i

135 these nuclear movement defects, dorsal actin cable flow was nondirectional in cells lacking emerin.

136 onstrate that miR-24 directly controls actin cable formation and cell mobility.

137 the in vivo regulatory mechanisms for actin cable formation are less clear.

138 Formins drive cable formation by promoting actin nucleation and by acc

139 ), both E-cadherin down-regulation and actin-cable formation fail, thus resulting in open epidermal g

140 w tropomyosins contribute mechanistically to cable formation has been unclear, but genetic studies de

141 gnaling, whereas the reduction in hyaluronan cable formation induced by V3 expression is mediated by

142 Actomyosin cable formation is accompanied by junctional rearrangeme

143 R1, but not BNI1, leads to severe defects in cable formation, polarized secretion, and cell growth, s

144 ering of formins at cell tips promotes actin cable formation.

145 y as Bud14 in regulating Bnr1-mediated actin cable formation.

146 metry, we identified components of the actin cables formed in yeast extracts, providing the basis for

147 ompletion of spinal closure is imminent, the cable forms a continuous ring around the neuropore, and

148 track that more closely resembles the actin cables found in vivo.

149 nd regulate the formation of radiating actin cables from this site.

150 ed link between NatB, tropomyosin, and actin cable function from yeast to human.

151 sophila embryo is mediated by apical F-actin cables generated by the formin-family protein Diaphanous

152 es are in constant dynamic turnover yet some cables grow from the bud neck toward the back of the mot

153 nurse cells, continuous filopodia-like actin cables, growing from the plasma membrane and extending t

154 gnaling defects, suggesting that the control cable has helical character.

155 Yet linking quantum-enabled devices with cables has proved difficult because most cavity or circu

156 crease in number in a model of fibrosis, and cables have unique interactions with collagen-producing

157 membrane helix (TM2), a five-residue control cable helix at the membrane-cytoplasm interface, and a f

158 up interface, causing a break in the control cable helix to attenuate the register mismatch and enhan

159 r localization of a supracellular actomyosin cable in the cells at the placode border, with myosin II

160 rs and belowground buried resistance heating cables in each of 72-7.0 m(2) plots.

161 es are delivered by myosin-V on linear actin cables in fission yeast cytokinesis.

162 t the activity of MyoVc to specialized actin cables in order to co-ordinate and target the final stag

163 ency of Myo52p-directed motility along actin cables in the cell.

164 cal region but not in the longitudinal actin cables in the shank.

165 ndergo processive movement along actin-Cdc8p cables in vivo.

166 r organelles for several microns along actin cables in vivo.

167 n of secretory vesicle transport along actin cables in yeast.

168 t the wound margin; contraction of the actin cable, in turn, closes the wound.

169 ire, multifilament form that can be wound or cabled into arbitrary geometries and will be especially

170 d to transform telecommunication fiber-optic cables into dense seismic arrays that are cost effective

171 Laser ablation shows that the cable is under increased tension, implying an active inv

172 A five-residue control cable joins TM2 to the HAMP AS1 helix and mediates confo

173 utput, whereas insertions at the TM2-control cable junction caused kinase-off output.

174 scale material geometries including anchors, cables, lattices and webs, as well as functional materia

175 f a negative feedback mechanism that detects cable length and prevents overgrowth.

176 we describe a novel molecular mechanism for cable length control inspired by recent experimental obs

177 redictions of the antenna mechanism of actin-cable length control.

178 activity is crucial in vivo for proper actin cable length, shape, and velocity and, in turn, efficien

179 We quantify animal-to-animal variability in cable lengths (CV = 0.4) and branching patterns in the G

180 We compute the probability distribution of cable lengths as a function of several experimentally tu

181 Cable-like copper oxide/carbon-nitride core-shell nanost

182 MSC comparatively, through the formation of cable-like hyaluronic acid structures.

183 Axons are cable-like neuronal processes wiring the nervous system.

184 form of HA (HC-HA) leads to the formation of cable-like structures that promote adhesion of leukocyte

185 observed and characterized two distinct Cdc8 cables loading and spreading cooperatively on individual

186 n V, Myo2, responds by relocalizing to actin cables, making it the fastest response documented.

187 as roads, rail tracks, pipelines, fences and cables, many of which divide the landscape and limit ani

188 d severely underestimates energy cost in the cable model by 20-70%.

189 Incorporation of nitrogen processes into the CABLE model decreased Xss in all biomes via reduced NPP

190 is model with an anatomically realistic axon-cable model of motoneurons, interneurons, and myelinated

191 Finally, a cable model of the OHC, which can match our data, indica

192 ptotic analysis of a two-compartment passive cable model, given a pair of time-dependent synaptic con

193 for a patch of membrane within a distributed cable model.

194 ommunity Atmosphere Biosphere Land Exchange (CABLE) model to help understand differences in modeled c

195 These actin cables move nuclei away from ring canals.

196 Introduction of Y79S restored cable movement to a more normal phenotype.

197 two formins, Bni1p and Bnr1p, assemble actin cables necessary for polarized cell growth and organelle

198 Thus Hof1 tunes formins to sculpt the actin cable network.

199 Assembly of appropriately oriented actin cables nucleated by formin proteins is necessary for man

200 n "superhighways" composed of parallel actin cables nucleated by formins from the plasma membrane [4]

201 The increase in cable number is accompanied by increased muscle stiffnes

202 A new cabled observatory atop Axial Seamount on the Juan de Fu

203 were captured in real time by a new seafloor cabled observatory, revealing the timing, location, and

204 spontaneous Ca release on a one-dimensional cable of cardiac cells.

205 Actin cables of budding yeast are bundles of F-actin that exte

206 ectrical wave propagation in one dimensional cables of healthy and failing cells.

207 h are oriented perpendicular to two parallel cables of the lateral element arranged at a distance of

208 ng F-actin, the structure of the tropomyosin cable on actin is uncertain.

209 g contraction of an intercellular actomyosin cable or to active cell migration, but the relative cont

210 nct spatial architecture of the apical actin cables (or actin cap) facilitates rapid biophysical sign

211 Myo52 may contribute to actin cable organization by delivering actin regulators to cel

212 ique that enables determinations of multiple cable parameters in action potential-firing fibres inclu

213 cells, would enhance leukocyte binding to HA cables produced in response to poly(I:C).

214 arising at least partly from differences in cable properties and the nonlinear behaviour of the resp

215 Macroscopic branching patterns and fine cable properties are variable within and across neuron t

216 at source estimation methods, as well as the cable properties of neurons, which all assume ohmic extr

217 of local field potentials, as well as on the cable properties of neurons.

218 Our findings suggest that cable properties play a central role in determining wher

219 would normally occur attributable to passive cable properties.

220 tensively reflect the influence of dendritic cable properties.

221 ed formation of the perinuclear apical actin cables protects the nuclear structural integrity from ex

222 The use of the cable-reconstitution system to test roles for the key ac

223 idue in the Tsr N-terminal linker or control cable reduces conformational heterogeneity at the N-term

224 We hypothesized that actin cables regulate the processive properties of MyoVc.

225 Myo2 immobilized on cables releases its secretory cargo, defining a new rigo

226 phobic amino acids at S217, the last control cable residue, produced attractant-mimic effects, most l

227 disrupt function at G213, the first control cable residue, which might serve as a structural transit

228 t alter the sidechain environment of control cable residues at the membrane core-headgroup interface,

229 e amino acid replacements at the Tsr control cable residues.

230 structural motifs in macroscopic materials (cables, ropes, and textiles) as well as synthetic and bi

231 lar F-actin network, which includes an actin cable running along the neural fold tips.

232 ide a comprehensive model of the tropomyosin cable running continuously on F-actin.

233 an autonomous underwater vehicle and a ship-cabled sampler.

234 e insertions or deletions in the TM2-control cable segment of Tsr.

235 ty by modulating the helicity of the control cable segment.

236 t alter actin levels in cables but, instead, cable shape and functionality.

237 the chemical nature and size of the control cable side chains are not individually critical for sign

238 As with a cable, spine neck resistance (R(neck)) increases with in

239 To explore control cable structural features important for signal transmiss

240 in low serum conditions, formation of the HA cable structure, increased anchorage-independent growth,

241 he increased "HA pool," formation of the "HA cable" structure, up-regulation of HA synthase-2, and CD

242 mmatory matrix leads to dissolution of HC-HA cable structures and abolishes leukocyte adhesion.

243 egoing mechanisms, the model generates actin cable structures and dynamics similar to those observed

244 r simulations reproduce the particular actin cable structures in myoVDelta cells and predict the effe

245 ated from control mice generated HA-enriched cable structures in the ECM, providing a substrate for m

246 s and organizes actin filaments into ordered cable structures.

247 smooth muscle cells produced spontaneous HA "cable" structures, without additional stimuli, that were

248 posed of discontinuous struts and continuous cables, such systems are only structurally stable when s

249 ormation of long microtubule-based cytosolic cables suggesting a role in microtubule formation and st

250 retrograde flow of dorsal perinuclear actin cables, supporting the recently proposed function for th

251 emission into the MRI scanner and prevented cable/surface pad heating during imaging, while preservi

252 perstructures are composed of dimeric double-cable tape-like structures that, in turn, are supercoile

253 advertising viewed on national broadcast and cable television in 2010 using a Nielsen panel of televi

254 . (2015) identifies an apicobasal actomyosin cable that characterizes apoptotic cells and contributes

255 flat indoor environment compatible with the cable that tethers the subject to recording instruments.

256 tail overlapping domain to form a continuous cable that wraps around the F-actin helix.

257 O2-induced ROS were found to decompose actin cables that are driving meiotic chromosome mobility, an

258 he assembly of an organized network of actin cables that direct polarized secretion.

259 quired for the assembly of an array of actin cables that facilitate polarized vesicle delivery and da

260 thesizing leukocyte-adhesive hyaluronan (HA) cables that remain attached to their cell surfaces.

261 ing is driven by contraction of actin/myosin cables that span cells at wound edges, and it is the pre

262 These actin filaments bundle to form actin cables that span the cell and guide the movement of vesi

263 ited from formin-Cdc12p nucleated long actin cables that were generated at multiple nonmedial locatio

264 In particular, we find that for a short cable the mean first passage time increases exponentiall

265 Furthermore, we find that for long cables the mean first passage time decreases as a power

266 ingle cell and spatially coupled homogeneous cable, the interplay between alpha and tau affects the d

267 home cells contained long longitudinal actin cables, the short Li1 fiber cells accumulated disoriente

268 Determination of lambda using cable theory assumes steady-state conditions.

269 We find that several important cable theory assumptions are violated when applied to sm

270 In contrast with classical cable theory predictions, the persistent sodium current

271 However, the applicability of cable theory to blood vessels depends on assumptions tha

272 ture have traditionally been described using cable theory, i.e., locally induced signals decaying pas

273 Based on cable theory, the unique 30 nm width compartment (the ex

274 -state length-constant, lambda, derived from cable theory.

275 as a descriptive measure and not in light of cable theory.

276 to activate host prothrombin and form fibrin cables, thereby promoting the establishment of infectiou

277 ndocytosis and strong stabilization of actin cables, thereby revealing a selective and previously una

278 into bundles forming helix-like cytoplasmic cables throughout the cell, and in a subset of cells add

279 promote formin-dependent nucleation of actin cables, thus expanding our understanding of how specific

280 motions might be relayed through the control cable to reach the input AS1 helix of HAMP by constructi

281 a perinuclear actin meshwork connects actin cables to nuclei via actin-crosslinking proteins such as

282 sported out of the daughter buds along actin cables to preserve youthfulness.

283 n addition, Myo52 motor activity may pull on cables to provide the tension necessary for their extens

284 nt assembly, as artificially tethering actin cables to the nuclear envelope via a Myo52 motor domain

285 The coupling of actin cables to the nuclear membrane for nuclear movement via

286 from coupling rearward-moving, dorsal actin cables to the nucleus by linear arrays of nesprin-2G and

287 Instead, we suggest that the Tsr control cable transmits input signals to HAMP by modulating the

288 lar to the cell surface or wrapped in coiled cables (two alternative models), the glycan strands in G

289 uple the nucleus to dorsal perinuclear actin cables undergoing retrograde flow.

290 y was performed, and the electrode array and cable were introduced into the eye via a pars plana scle

291 interactions between ECM cells and collagen cables were also observed and reconstructed by serial bl

292 A pulse generator and two extension cables were implanted in a second surgery 3-4 weeks late

293 effects of increased gait stability once the cables were removed.

294 late Rok, thus preventing the formation of a cable where Crumbs and aPKC are localized.

295 s that collagen is organized into perimysial cables which increase in number in a model of fibrosis,

296 Vs transport secretory vesicles along actin cables, which are dynamic actin bundles assembled by the

297 the polarity regulator Cdc42p orients actin cables, which deliver vesicles carrying Cdc42p to the po

298 In S. cerevisiae, formins assemble actin cables, which serve as tracks for myosin-dependent intra

299 lls between fingers contain continuous actin cables, which were also determined to contain myosin IIA

300 sion results in externalization of conductor cables, with a higher risk of electrical failure.