ライフサイエンスコーパス: barb

1 n in the corresponding region of the feather barb.

2 quasi-ordered nanostructures in bird feather barbs.

3 the actin-capping protein (CP) gelsolin from barbed actin ends in vitro, allowing for elongation of a

4 supporting the developmental hypothesis that barbs already possessed barbules when they fused to form

5 ervation to demonstrate that VopL/F bind the barbed and pointed ends of actin filaments but only nucl

6 - and thymosin-beta4-bound G-actin, and free barbed and pointed ends of actin filaments by model fitt

7 ts the monomer dissociation rate at both the barbed and pointed ends of actin.

8 r severing and accelerated monomer loss from barbed and pointed ends.

9 that Tbeta4 has two helices that bind at the barbed and pointed faces of G-actin, preventing the inco

10 nd the spectrin-based membrane skeleton, use barbed and pointed-end capping proteins to control subun

11 bit a short, slender rachis with alternating barbs and a uniform series of contiguous barbules, suppo

12 Each spicule is covered with recurved barbs and has an internal architecture consisting of a s

13 tively remove the surface contamination from barbs and shafts, and therefore, it is necessary to deve

14 Here, I call attention to these ethical barbs and suggest a way in which to proceed cautiously.

15 hered in areas where a high density of small barbs are present and then quickly transported to the le

16 Barbs at the tip of the quill independently exhibit the

17 -Saharan speakers hunting aquatic fauna with barbed bone points occupied the southern Sahara, while p

18 ws that nanostructure in single bird feather barbs can be varied continuously by controlling the time

19 extensive thickening of the carotenoid-laden barb cortex, producing the yellow crown coloration.

20 ion of the Arp2/3 complex with CK666 reduced barbed end actin assembly site density at the leading ed

21 sistant to cytochalasin D that inhibits fast barbed end actin assembly.

22 her proteins, including formins, bind at the barbed end and allow filament growth.

23 agonizes CP by reducing its affinity for the barbed end and by uncapping CP-capped filaments, whereas

24 within dendritic spines, as revealed by free-barbed end and FRAP assays, consistent with a role for E

25 ly accessible site on CP bound to a filament barbed end and inducing a change in the conformation of

26 ent nucleation then remain on the elongating barbed end and modulate filament elongation.

27 G-actin in 1:2 complexes that participate in barbed end assembly.

28 in complexes and deliver them rapidly to the barbed end associated with the FH2 domain.

29 Saturating phosphate increases the barbed end association rate constant of Mg-ADP-actin 15%

30 ding but promote high affinity (K(d) = 9 nM) barbed end attachment.

31 how two actin regulators, capping protein, a barbed end binding protein, and the Arp2/3 complex, a po

32 Surprisingly, neither mutation abolishes barbed end binding, as judged by pyrene-actin and total

33 Further, mDia1 displaced from the barbed end by CP can randomly slide along the filament a

34 nd modulates formin-dependent capping of the barbed end by relieving inhibition of elongation by FRL1

35 vitro; instead, they were proposed to act as barbed end cappers or filament bundlers.

36 hese results can explain how V-1 inactivates barbed end capping by CP and why V-1 is incapable of unc

37 Here we show that in the mouse cochlea the barbed end capping protein twinfilin 2 is present at the

38 K113E actin polymerization, consistent with barbed end capping.

39 evering, whereas G1 and G2 were required for barbed end capping.

40 ong electrostatic binding site for CP on the barbed end compete for this basic patch on CP.

41 3 increased, with the half-time of CP at the barbed end decreasing from approximately 30 min without

42 V, VC, and VCA enhance barbed end depolymerization like profilin but neither nu

43 ofilin with the FH1 domain speeds processive barbed end elongation by FH2 domains.

44 combined inhibition of actin nucleation and barbed end elongation by profilin and SpTm.

45 tary mechanisms that regulate actin filament barbed end elongation in Arp2/3-derived networks.

46 atial and temporal control of actin filament barbed end elongation is crucial for force generation by

47 inus inhibits actin polymerization and slows barbed end elongation with moderate affinity.

48 over actin subunits through a combination of barbed end elongation, severing, and WH2 motif-mediated

49 ional proteins that work together to inhibit barbed end elongation.

50 ers and displays high affinity inhibition of barbed end elongation.

51 ex with cortactin that blocks actin filament barbed end elongation.

52 assay for Drosophila embryos, which revealed barbed end enrichment at junctions.

53 y remaining processively associated with the barbed end for an average of approximately 10 s in solut

54 may explain the inhibitory effects of PKD on barbed end formation as well as on directed cell migrati

55 ion to activate cofilin, promotes actin free barbed end formation, accelerates actin turnover, and en

56 After barbed end formation, cortactin is dephosphorylated, whi

57 small inhibitory RNA abrogates enhanced free barbed end formation, increased actin polymerization, an

58 bsequent Rac activation increases actin free barbed end formation.

59 n by promoting actin polymerization via free barbed end generation and centripetal elongation of an F

60 The C helix is likely to bind to the barbed end groove of Arp3 in a position for VCA to deliv

61 GSNL-1 severs actin filaments and caps the barbed end in a calcium-dependent manner similar to that

62 SNL-1 severed actin filaments and capped the barbed end in a calcium-dependent manner.

63 actin cytoskeletal polarity by developing a barbed end incorporation assay for Drosophila embryos, w

64 Each FH1 domain transfers actin to the barbed end independently of the other and structural evi

65 es showed that the binding of formins to the barbed end induces conformational transitions in actin f

66 ting from one end and developing towards the barbed end might be involved in force generation and dir

67 They attach to the barbed end of a filament and prevent polymerization, lea

68 sis shows how the binding of profilin to the barbed end of actin causes a rotation of the small domai

69 heads swing forward alternately towards the barbed end of actin driven by ATP hydrolysis.

70 formin, AtFH14, processively attaches to the barbed end of actin filaments as a dimer and slows their

71 s, function as homodimers that bind with the barbed end of actin filaments through a ring-like struct

72 CP binds with high affinity to the barbed end of actin filaments, blocking the addition and

73 of the actin cytoskeleton by binding to the barbed end of actin filaments.

74 ittle effect on Capu once it is bound to the barbed end of an elongating filament.

75 ivation the first actin monomer binds at the barbed end of Arp2.

76 ently inhibits nucleation and binding to the barbed end of elongating filaments by the C-terminal hal

77 brin inhibits depolymerization mainly at the barbed end of F-actin.

78 It binds to the barbed end of filaments with high affinity and modulates

79 elerate elongation, although it binds to the barbed end of filaments.

80 ofilin-actin from the cellular pool onto the barbed end of growing filaments.

81 %) associate for approximately 25 s with the barbed end of preassembled filaments, inhibiting their e

82 expressed, 62-kDa heterodimer that binds the barbed end of the actin filament with approximately 0.1

83 heterodimeric 62-kDa protein that binds the barbed end of the actin filament with high affinity to b

84 and the molecular basis for how CP binds the barbed end of the actin filament, we have used a combina

85 fidelity of information communicated at the barbed end of the actin filament.

86 rmin Homology 2 (FH2) domain dimers with the barbed end of the filament, allowing subunit addition wh

87 P interacts with both actin protomers at the barbed end of the filament, and the amphipathic helix at

88 in complexes into contact with the FH2-bound barbed end of the filament, thereby enabling direct tran

89 in is proposed to be in position to join the barbed end of the growing filament concurrently with the

90 st G-actin compared with muscle actin in the barbed end pivot region and areas in subdomains 1 and 2

91 The barbed end rate constants for mouse capping protein (CP)

92 nal tail from a hydrophobic groove at Arp3's barbed end to destabilize the inactive state, providing

93 and it subsequently displaces Spire from the barbed end to elicit rapid processive assembly from prof

94 e along the filament and later return to the barbed end to re-form the complex.

95 ne-dimensional diffusion, and (3) processive barbed end tracking.

96 ults offer a mechanistic explanation for the barbed end uncapping activity of CARMIL, and they identi

97 in-profilin interface, Ala(167) of the actin barbed end W-loop and His(372) near the C terminus form

98 processively associated with the elongating barbed end while driving the addition of profilin-actin.

99 processively associated with the elongating barbed end while facilitating the addition of profilin-a

100 has a small but measurable affinity for the barbed end, as inferred from previous studies and kineti

101 ow that CAH3 binds CP already present on the barbed end, causing a 300-fold increase in the dissociat

102 ersistently associated with the fast-growing barbed end, enabling rapid insertion of actin subunits w

103 ns tunes the processive association with the barbed end, indicating that this is a general role for f

104 s actin filament assembly and remains at the barbed end, modulating elongation.

105 depolymerization of the pointed end than the barbed end, suggesting a weak affinity of phosphate near

106 eas several proteins cap the rapidly growing barbed end, tropomodulin (Tmod) is the only protein know

107 While several proteins cap the barbed end, tropomodulins (Tmods), a family of four clos

108 ation during translocation along the growing barbed end, we propose that the flexible linker influenc

109 otein, competes with FH1-FH2 at the filament barbed end, where its binding is mutually exclusive with

110 tue of its ability to cap the actin filament barbed end, which promotes Arp2/3-dependent filament nuc

111 ses that deliver multiple actin monomers per barbed end-binding event and effectively antagonize fila

112 d actin polymerization protein Arp3, and the barbed end-capping and bundling protein Eps8, illustrati

113 association of CP with and affinity for the barbed end.

114 on to and high affinity interaction with the barbed end.

115 filaments or by dissociating Cdc12p from the barbed end.

116 AtFH14 moves processively on the elongating barbed end.

117 de novo and stay associated with the growing barbed end.

118 the ability of capping protein to block the barbed end.

119 1-mediated transfer of actin subunits to the barbed end.

120 w that tropomyosin regulates dynamics at the barbed end.

121 vitro to render it incapable of binding the barbed end.

122 ation of actin-binding regions of FH2 to the barbed end.

123 of the formin mDia1 simultaneously bind the barbed end.

124 associating with, and dissociating from, the barbed end.

125 nto a version with moderate affinity for the barbed end.

126 n lifetime when force was applied toward the barbed (+) end.

127 the absence of profilin, but profilin slows barbed-end acceleration from constructs containing the P

128 Adducin functions as a barbed-end actin capping protein to regulate actin filam

129 factors Diaphanous and Enabled both promote barbed-end actin polymerization and can stimulate filopo

130 clustered N-WASP affects Arp2/3-independent barbed-end assembly.

131 ology 1 (FH1) domain from one formin and the barbed-end associated FH2 domain from the other formin,

132 lin-actin with the FH1 domain as well as the barbed-end associated FH2 domain.

133 Point mutagenesis reveals that reducing the barbed-end binding activity of FRL1 and mDia2 greatly en

134 ith a requirement of accelerated assembly on barbed-end bundling.

135 omain regulate actin assembly and processive barbed-end capping by the FH2 domain.

136 CapZ and cytochalasin D (CytoD), a barbed-end capping drug, strongly inhibit bursting disas

137 /CD2AP and a previously unrecognized role of barbed-end capping in junctional actin dynamics.

138 has not been defined, although severing and barbed-end capping of actin filaments have been proposed

139 Mena, an actin barbed-end capping protein antagonist, is expressed as v

140 iated protein (FSGS3/CD2AP) as a novel actin barbed-end capping protein responsible for actin stabili

141 way substrate 8 (Eps8; an actin bundling and barbed-end capping protein) and actin-related protein 3

142 orescence microscopy, we found that ABP29, a barbed-end capping protein, competes with FH1-FH2 at the

143 rk assembly at the leading edge by promoting barbed-end capping there.

144 reated by complex exchange slows the rate of barbed-end elongation by rapidly associating with, and d

145 concentrations (0.5-25 microM), the rate of barbed-end elongation increases with the number of polyp

146 at the N-terminal ABD1 blocks actin filament barbed-end elongation, whereas ABD2 and ABD3 do not show

147 lament, whereas profilin:actin only supports barbed-end elongation.

148 that interact with each other for processive barbed-end elongation.

149 other and together accelerate actin filament barbed-end elongation.

150 inding protein profilin-increase the rate of barbed-end elongation.

151 Cytochalasin-D inhibition of barbed-end exchange reduces rhodamine-actin incorporatio

152 ruitment of actin-capping protein, revealing barbed-end filament capping at endocytic sites to be a r

153 tactin phosphorylation and cofilin-dependent barbed-end formation at invadopodia, leading to a signif

154 nts of the phosphate clamp, cleft mouth, and barbed-end groove, providing a way for changes in the nu

155 in polymerization ~18 times faster than free-barbed-end growth while simultaneously enhancing protect

156 alphaE-catenin ABD binding limits barbed-end growth, especially in actin filament bundles.

157 or DCC, interacts with and ubiquitinates the barbed-end polymerase VASP to modulate filopodial stabil

158 patially distributed model, both synergy and barbed-end production are significant over a range of ac

159 Furthermore, barbed-end production is greatest when Arp2/3 activation

160 We specifically consider key barbed-end regulators such as capping protein and formin

161 Binding of open II vinculin to the barbed-end suggests this conformation allows for vinculi

162 a population of reversed filaments with the barbed-end toward the cell center.

163 tment of peripheral filaments and continuous barbed-end turnover.

164 ts by interacting with both S1 and S3 of the barbed-end, using the surface of Vt normally occluded by

165 at tension is generated by myosin pulling on barbed-end-anchored actin filaments in a stochastic slid

166 dent actin depolymerization factor and not a barbed-end-capping factor as was previously thought.

167 We show that myosin 15-S1 is a barbed-end-directed motor that moves actin filaments in

168 partly invaginated CCSs with actin filament barbed ends abutting the CCS neck, to a polarized comet

169 ments, whereas capping protein (CP) binds to barbed ends and arrests polymerization.

170 Capping protein (CP) is known to regulate barbed ends and control actin assembly in cells.

171 at Lpd delivers Ena/VASP proteins to growing barbed ends and increases their polymerase activity by t

172 homology 2 (FH2) domain that binds filament barbed ends and is critical for polymerization and depol

173 mechanism by which Spire and Fmn2 compete at barbed ends and the role of FSI in orchestrating this co

174 s revealed an aster of actin filaments whose barbed ends are focalized near the plasma membrane.

175 nched actin network, in which actin filament barbed ends are oriented toward the CCS.

176 rsing melanosomes along actin tracks whose +/barbed ends are oriented toward the plasma membrane.

177 ccurs only at low activation rates, when few barbed ends are produced.

178 in-filament barbed ends, and both N-WASP and barbed ends are tightly clustered in these invasive stru

179 In addition, FSI binds actin at filament barbed ends as a weak capper and plays a role in displac

180 cofilin can sever actin filaments to create barbed ends at invadopodia to support Arp2/3-dependent a

181 Newly generated actin free barbed ends at the front of motile cells provide sites f

182 by itself associates very poorly to filament barbed ends but is rapidly recruited to Spire-capped bar

183 ng influence on dissociation of formins from barbed ends but only a weak effect on elongation rates.

184 filopodia of uniform thickness with aligned barbed ends by a unique mechanistic cycle.

185 d lamellipodial assembly features capping of barbed ends by CP, and the formation of filopodia is pro

186 Individual barbed ends captured by WWCA domains grow at or below th

187 Moreover, in these processes, barbed ends directly push onto the load, as in a convent

188 berrant regulation of F-actin and actin free barbed ends dynamics.

189 runs, allowing them to catch up with leading barbed ends efficiently.

190 ivity of cofilin, a protein that creates new barbed ends for actin filament elongation, amplifies and

191 ctin assembly and protected growing filament barbed ends from capping protein.

192 for estimation of the concentration of free barbed ends from pyrene intensity curves.

193 New growth at barbed ends generated by severing was blocked specifical

194 Rapid polymerization of actin filament barbed ends generates protrusive forces at the cell edge

195 Dissociation of formins from barbed ends growing in the presence of profilin is propo

196 s remarkably slow and restricted to filament barbed ends in a small tip compartment, with minimal acc

197 ament length and for the capture of filament barbed ends in cells.

198 otein (CP), a major capper of actin filament barbed ends in cells.

199 Ena-associated trailing barbed ends in Fascin-bundled actin filaments have appro

200 drive the processive elongation of filament barbed ends in membrane protrusions or at the surface of

201 embly in which any cluster of actin filament barbed ends in proximity to the plasma membrane, either

202 The affinity of fission yeast CP for barbed ends is a thousandfold less than mouse CP, becaus

203 The regulation of free barbed ends is central to the control of dynamic actin a

204 force, interactions between WH2 domains and barbed ends may locally amplify signals for dendritic ac

205 opodial base and diffuse toward the filament barbed ends near the tip.

206 he cell allow capping protein to bind to the barbed ends of actin filaments and Arp2/3 complex to bin

207 concentration of capping protein, which caps barbed ends of actin filaments and prevents elongation,

208 muscles near or on sarcomere Z lines, where barbed ends of actin filaments are anchored.

209 ing proteins bind to and dissociate from the barbed ends of actin filaments by observing single muscl

210 The barbed ends of actin filaments in striated muscle are an

211 e interaction of N-WASP with GRB2 and/or the barbed ends of actin filaments increases its exchange ra

212 min proteins associate processively with the barbed ends of actin filaments through many rounds of ac

213 also demonstrate that Aip1 does not cap the barbed ends of actin filaments, as was previously though

214 VASP induces and maintains clustering of the barbed ends of actin filaments, which putatively corresp

215 Myosin-5 walks toward the barbed ends of F-actin, traveling to sites of actin poly

216 Aip1 does not cap the barbed ends of filaments severed by cofilin.

217 Capping protein (CP) binds to barbed ends of growing actin filaments and inhibits elon

218 ngly, a loss of the uniform alignment of the barbed ends of the actin filaments.

219 ion due to addition of actin monomers to the barbed ends of the filaments.

220 ing nurse cell dumping, Enabled localizes to barbed ends of the nurse cell actin filaments, suggestin

221 nd Arp2/3 can each generate a large pulse of barbed ends on their own, but have little synergy; high

222 een inferred that the regulation of filament barbed ends plays a central role in choreographing actin

223 and promotes its displacement from filament barbed ends providing insight into possible modes of coo

224 gonizes capping protein but dissociates from barbed ends relatively quickly.

225 ly less effective at processively elongating barbed ends than most well studied formins.

226 Cdc12p allows barbed ends to elongate in the presence of excess cappin

227 ment by transiently attaching actin filament barbed ends to the membrane.

228 ulin restricts the position of thin filament barbed ends to the Z-disc via a direct interaction with

229 filaments are uniformly oriented with their barbed ends toward stereocilia tips.

230 recently demonstrated how Spire, which caps barbed ends via its WH2 domains, activates Fmn2.

231 nds but is rapidly recruited to Spire-capped barbed ends via the KIND domain, and it subsequently dis

232 d, with mDia1 moving processively on growing barbed ends while APC remained at the site of nucleation

233 eing rapidly polymerized by formins at their barbed ends while simultanteously being stochastically s

234 arms to processively track growing filament barbed ends while three G-actin-binding sites (GABs) on

235 tivating Arp2/3, N-WASP binds actin-filament barbed ends, and both N-WASP and barbed ends are tightly

236 resulting from addition of monomers to free barbed ends, and one with slow turnover dynamics with po

237 duce a rapid biphasic increase in actin free barbed ends, and we found both phases absent in fibrobla

238 te, and bundle filaments by associating with barbed ends, as well as in their use of WH2 motifs and o

239 zed filaments shrink rapidly, primarily from barbed ends, at 1.8/s, but as they age they switch to a

240 nd PI(3,4,5)P(3), prevent CP from binding to barbed ends, but three different assays showed that none

241 Two important regulators of free barbed ends, cofilin and Arp2/3, have been shown to work

242 tes dissociation of FH2 domains from growing barbed ends, FH2 domains must pass through a state that

243 ts Fmn2 and facilitates its association with barbed ends, followed by rapid processive assembly and r

244 sembly of actin filaments that grow at their barbed ends, independent of eukaryotic factors.

245 itate the localized generation of free actin barbed ends, leading to membrane protrusion.

246 athway where filaments grow transiently from barbed ends, rapidly terminate growth to enter a long-li

247 by interacting directly with actin filament barbed ends, recruiting profilin-actin, and blocking cap

248 We show that by capping filament barbed ends, Spire recruits Fmn2 and facilitates its ass

249 drugs that release mDia1 from actin filament barbed ends, stimulated stable MT formation in serum-sta

250 Capping protein (CP) binds to free barbed ends, thereby arresting microfilament growth and

251 tivity, and elevated formation of actin free barbed ends, thus restoring normal beta(2) integrin func

252 Ena/VASP proteins regulate actin dynamics at barbed ends, we monitored individual actin filaments gro

253 Drosophila Fhod binds tightly to barbed ends, where it slows elongation in the absence of

254 gather and simultaneously elongate multiple barbed ends.

255 mn2 alternately kick off each other from the barbed ends.

256 opodia-like F-actin networks without tapered barbed ends.

257 vivo, and is proposed to cap actin filament barbed ends.

258 nishing the filament subpopulation with free barbed ends.

259 (CAPZ), which blocks actin polymerization at barbed ends.

260 rization of actin filaments by capping their barbed ends.

261 ation of active ADF/cofilin and free F-actin barbed ends.

262 In addition, the C terminus binds filament barbed ends.

263 g activity of cofilin to generate actin-free barbed ends.

264 o control cofilin's generation of actin-free barbed ends.

265 port of G-actin monomers to the polymerizing barbed ends.

266 and delivering ATP-actin to growing filament barbed ends.

267 in-mediated processive elongation of growing barbed ends.

268 y displaces the Bnr1 FH2 domain from growing barbed ends.

269 ermediates with lowered affinity for CapZ at barbed ends.

270 oated surfaces via interactions with growing barbed ends.

271 wever, CYK-1 rapidly re-associates with free barbed ends.

272 n, helps to maintain Ena/VASP at the growing barbed ends.

273 s at concentrations that block CP binding to barbed ends.

274 cement of filament growth from newly created barbed ends.

275 mote flux of subunits through actin filament barbed ends.

276 hange and delivery of subunits onto filament barbed ends.

277 ormin homology 2 (FH2) domains with filament barbed ends.

278 rocessively associated with the fast-growing barbed ends.

279 ing and remains bound to the newly generated barbed ends.

280 estering actin monomers and capping filament barbed ends.

281 and restraining elongation to remaining free barbed ends.

282 ely active, diffusing freely to find and cap barbed ends.

283 han the diffusion-limited rate of unattached barbed ends.

284 Localization of Fhos to the barbed-ends of the arrays, achieved via a novel N-termin

285 The dynamics of the barbed, fast-growing end of the filament are controlled

286 trollers for the topologies of rachidial and barb generative zones (setting vane boundaries), respect

287 e adhesion force and the cooperation between barbs in the 0-2 mm and 2-4 mm regions appears critical

288 Barbs located near the first geometrical transition zone

289 l organization of the keratin matrix feather barbs of the crown.

290 y developed slightly but significantly fewer barbs on their stings (-7% in the 40K-treated bees).

291 ing whether they associate with the filament barbed or pointed end.

292 During exocytosis, the barbed part of the tubule is accelerated with >5 million

293 The intermediate nature of the crown barbs, resulting from past admixture appears to have ren

294 In developing flight-feather follicles, the barb ridges are organized helically toward the anterior

295 Dynamic scaling analysis of the single barb scattering data implies that the phase separation a

296 netration and high tissue adhesion where the barbs specifically contribute to adhesion and unexpected

297 Plants and animals use plumes, barbs, tails, feathers, hairs and fins to aid locomotion

298 ature microscopic backward-facing deployable barbs that are used in self-defense.

299 that the force transmitted from the surface barbs to the remainder of the skeletal system was maximi

300 The dual functions of barbs were reproduced with replica molded synthetic poly