ライフサイエンスコーパス: F-actin

1 tions with nucleotide and filamentous actin (F-actin).

2 of the contractile ring, filamentous actin (F-actin).

3 between the bacterium and filamentous actin (F-actin).

4 rce generated by transient associations with F-actin.

5 e isoform of human cofilin 2 (CFL2) bound to F-actin.

6 he intermolecular interface between CFL2 and F-actin.

7 alization of YAP which led to an increase in F-actin.

8 yosin does not block myosin binding sites on F-actin.

9 range of actin-associated proteins bound to F-actin.

10 ER-PM junctions that is in part regulated by F-actin.

11 ells and fibrosarcoma cells independently of F-actin.

12 cues of axon guidance like neuropilin-1 and F-actin.

13 el of the vinculin tail (Vt) domain bound to F-actin.

14 A303R) had no effect on the interaction with F-actin.

15 gies, but have the same skeleton composed of F-actin.

16 oes not bind beta-catenin but interacts with F-actin.

17 protein translation, and increased levels of F-actin.

18 w that each ABS binds to a distinct place on F-actin.

19 r (4.6 A) and Mg-ADP (5.5 A) states bound to F-actin.

20 by altering the subcellular distribution of F-actin.

21 architecture is similar to that of mammalian F-actin.

22 we observed depolymerization of synaptosomal F-actin accompanied by increased globular-actin (G-actin

23 We show that INFT-2 promotes F-actin accumulation in the EC, and that CYK-1 inhibits

24 ve changes thus led to a dis-organization of F-actin across Sertoli cell cytosol, causing truncation

25 myosin II delayed furrow initiation, slowed F-actin alignment, and reduced maximum contraction speed

26 ned focal adhesion maturation and associated F-actin alignment, consequently orchestrating anisotropi

27 In mammalian COS-7 cells, microtubules and F-actin also counteract each other to distribute POs.

28 ocytosis in SMN-knockdown cells by elevating F-actin amounts and rescued the axonal truncation and br

29 ed eosinophils to polarize with filamentous (F)-actin and granules at one pole and the nucleus in a s

30 exhibit dynamic accumulations of junctional F-actin and an increase in AJ protein levels.

31 ively intact, albeit more apically localized F-actin and BTB tight junctional proteins.

32 ading process nanoscale architecture wherein f-actin and drebrin intervene between microtubules and t

33 42 and its depletion leads to a reduction in F-actin and E-cadherin at junctions and a weakening of c

34 to IQGAP1 and thus higher levels of cortical F-actin and enhanced cell-cell adhesion.

35 CCL2 by disrupting polarized distribution of F-actin and Gbeta protein.

36 n maintaining the morphological structure of F-actin and in protein transport, loss of this function

37 e a feed-forward signaling mechanism wherein F-actin and integrin receptors drive contact formation b

38 tral domain inhibits the depolymerization of F-actin and is also responsible for oligomerization of T

39 and super-resolution microscopy to visualize F-actin and lytic granules in normal and LYST-deficient

40 The F-actin and myosin IIA were identified as coprecipitates

41 ganization at the ZA, accompanied by loss of F-actin and NMIIA, whereas ROCK2 knockdown had no signif

42 d activation of the PI3K, and recruitment of F-actin and of the actin-branching protein cortactin.

43 Both AICAR and metformin reduced F-actin and significantly reduced the fiber cross alignm

44 tes actin polymerization by interacting with F-actin and the actin effectors Ena/VASP proteins and th

45 The structure of cofilin on F-actin and the details of the intermolecular interface

46 Thus, reservoir F-actin and, consequently, reservoir dynamics are regula

47 e structure is defined by filamentous actin (F-actin) and we observed depolymerization of synaptosoma

48 radient sensing, excessive polymerization of F actin, and subsequent defective chemotaxis.

49 sins basal ATPase activity in the absence of F-actin, and (2) that the dynamic formation of the K265-

50 orphology of dendritic spines via regulating F-actin arborization.

51 urther functional assays suggest that intact F-actin architecture is required for phosphatidylinosito

52 recruitment of vinculin, alpha-catenin, and F-actin as a function of stiffness, as well as the dynam

53 fied ACF7, a crosslinker of microtubules and F-actin, as an essential player in this process.

54 asite load is associated with an increase in F- actin assembly and NADPH oxidase activity.

55 ith phosphoinositide-rich membranes, whereas F-actin assembly factors Dia2 and N-WASP reside on phosp

56 tion of the Arp2/3 complex or Rac attenuated F-actin assembly near bead binding sites, decreased the

57 of chemotactic behavior, including enhanced F-actin assembly, disturbed cell polarity, and increased

58 n as well as for TCR-driven WASp activation, F-actin assembly, immune synapse formation, actin foci f

59 iaphanous formin-mediated filamentous actin (f-actin) assembly, which drive ring constriction.

60 in Peanut and distribution of Diaphanous and F-actin at furrows.

61 ur genetic data suggest act as inhibitors of F-actin at the contractile ring.

62 gers full excitation of Ras and subsequently F-actin at the side of the cell facing the chemoattracta

63 We demonstrate that F-actin automata implement OR, AND, XOR and AND-NOT gate

64 alf-adder and controlled-not circuits in the F-actin automata.

65 molecule as an excitable automaton network (F-actin automaton).

66 oles, we directly compared their G-actin and F-actin binding affinities, and quantified the actin fil

67 myosin motor domain that are triggered upon F-actin binding and contribute critically to the mechano

68 alphaT286D mutant, indicating that transient F-actin binding contributes to the synaptic localization

69 IP-iLID can be used to temporally recruit an F-actin binding domain to MT plus ends and cross-link th

70 eneity suggests that CaMKII adopts different F-actin binding modes, which is most easily rationalized

71 Further, we show that the F-actin binding protein cortactin binds the PLS and is r

72 horylation of Y573 influences association of F-actin binding protein cortactin to MT1-MMP-positive en

73 iochemical analysis revealed CORO1C, another F-actin binding protein, whose direct binding to PLS3 is

74 c autophosphorylation states, also abolished F-actin binding.

75 kinase domains are joined via a linker to an F-actin-binding domain (FABD).

76 minal domain to wedge apart the membrane and F-actin-binding domains of ezrin.

77 rates WH2 domain functions with those of the F-actin-binding protein Abp1.

78 We recently found that the F-actin-binding protein afadin is required for lumen con

79 des a 139-amino-acid protein containing five F-actin-binding sites and two G-actin-binding sites, and

80 lease gates a transition from weak to strong F-actin-binding states.

81 colocalization of endosomal SDPN-1 with the F-actin biosensor Lifeact, and found that loss of SDPN-1

82 ests that the directionality of the vinculin-F-actin bond could establish long-range order in the act

83 er, how mechanical load affects the vinculin-F-actin bond is unclear.

84 action of time that NM-2B spends in strongly F-actin-bound states during ATP turnover.

85 d promote the formation of three-dimensional F-actin bundles.

86 or bundling, ABS1 contributes to the overall F-actin bundling activity of anillin and enables anillin

87 Fascin is an F-actin-bundling protein shown to stabilize filopodia an

88 Vinculin has binding sites for talin and F-actin, but effective binding requires vinculin activat

89 a conserved domain that can bind and bundle F-actin, but the importance and molecular details of its

90 E-cadherin stability depends on F-actin, but the mechanisms regulating actin polymerizat

91 1, and Adf1 all compete for association with F-actin by different mechanisms, and their cooperative a

92 th OEA and PEA were stained for cytoskeletal F-actin changes and lysed for immunoassay.

93 growth cones, it is unclear whether similar F-actin-clutching forces affect axon outgrowth and guida

94 F-actin co-localized with mesenchymal smooth muscle epit

95 Here, we report a 6.9 A cryo-EM structure of F-actin complexed with the L253P ABD.

96 d, and glass, suggesting different levels of f-actin composition.

97 paired endocytosis and a markedly diminished F-actin content at the base of the cups.

98 sent in cones and displayed markedly reduced F-actin content in rods, suggesting that protocadherin-1

99 th the basal and activated states, increased F-actin content, and increased the basal intracellular c

100 umber of ghost boutons, active zone density, F-actin content, and the formation of filopodia.

101 We also demonstrate that loss of synaptic F-actin contributes directly to memory deficits.

102 ization: the surprising increase in the peak F-actin count caused by reduced regulator branching acti

103 n, the motor domains of myosins, and a major F-actin crosslinker.

104 ing evidence suggests close coupling between F-actin cytoskeletal organization and nuclear morphology

105 nect the extracellular matrix (ECM) with the F-actin cytoskeleton and transduce mechanical forces gen

106 quires septin-dependent reorientation of the F-actin cytoskeleton at the base of the infection cell,

107 ontacts between the CaMKII dodecamer and the F-actin cytoskeleton that stabilize the initial weak (mi

108 F-actin decrease correlated inversely with increasing AD

109 ively targeting mitochondria, lysosomes, and F-actin demonstrate low toxicity and enable stimulated e

110 bonds increased under mechanical force in an F-actin-dependent manner, which could enable the capture

111 he Arp2/3 complex, which activation leads to F-actin--dependent bacterial internalization.

112 nstruction microscopy (dSTORM), we show that F-actin depolymerization in spines leads to a breakdown

113 Further, the F-actin-depolymerizing agent latrunculin induced recall

114 af cells lacked interdigitation of lobes and F-actin did not uniformly decorate the nuclear envelope.

115 atenin, which indirectly links E-cadherin to F-actin, did not decrease L. monocytogenes invasion of e

116 oli cell injury by rescuing the PFOS-induced F-actin dis-organization.

117 th-promoting signaling pathway amplifies the F-actin disassembly and repulsive effects of a growth-pr

118 h cofilin, Mical oxidation of actin promotes F-actin disassembly independent of the nucleotide-bound

119 emonstrate that synaptic dysfunction seen as F-actin disassembly occurs very early, before onset of p

120 s to combinatorially increase Mical-mediated F-actin disassembly, cellular remodeling, and repulsive

121 in's M44 and M47 residues to induce cellular F-actin disassembly.

122 cal to directly amplify Mical Redox-mediated F-actin disassembly.

123 stimulate such negative cellular effects as F-actin disassembly/repulsion.

124 on, we identified an interaction between the F-actin-disassembly enzyme Mical and the Abl tyrosine ki

125 he initiator caspase dronc triggers cortical F-actin dismantling, enabling the glands to stretch as t

126 larized with PSGL-1 at the nucleopod tip and F-actin distributed diffusely at the opposite end.

127 The method treats the time evolution of the F-actin distribution in three dimensions, with branching

128 universally, whereas chemical disruption of F-actin does so selectively.

129 d with disrupted organization of endothelial F-actin, downregulated expression of occludin and remode

130 esponse factor that responds to changes in G:F actin dynamics.

131 nstream of the Ras protein RasC, controlling F-actin dynamics and cAMP production.

132 y was tested as a novel tool for visualising F-actin dynamics in Toxoplasma gondii.

133 es septin-dependent, NADPH oxidase-regulated F-actin dynamics to organize the appressorium pore and f

134 ion of PAK1/2 and ERK/JNK MAPK signaling and F-actin dynamics.

135 vide a robust new tool for imaging parasitic F-actin dynamics.

136 Cortical F-actin elevation increased membrane E-cadherin, beta-ca

137 during furrow maturation, including abnormal F-actin enrichment and microtubule reorganization.

138 Live imaging revealed Rac-dependent F-actin enrichment at sites of EphB2 internalization, bu

139 pha-smooth muscle actin, pro-collagen 1, and F-actin expression.

140 -401-dependent modulation of PMN chemotaxis, F-actin expression/distribution, and actin-regulating pa

141 stress fibers, caused redistribution of more F-actin fibers to the cell periphery, and promoted sprea

142 found that AMPK induced depolymerization of F-actin (filamentous actin).

143 are unusual, permitting only short, unstable F-actin filaments.

144 de a detailed portrait of the EAAR including F-actin flow, the contribution of myosin contraction, an

145 ermore, cell adhesion proteins that utilized F-actin for attachment became properly distributed at th

146 aled that the adhesion molecule vinculin and F-actin form a catch bond that is dependent on the direc

147 nd activates Rho GTPases, which then induces F-actin formation.

148 ing the hMSC migration through mtROS-induced F-actin formation.

149 atopic and asthmatic donors; (iii) enhanced F-actin formation; (iv) marked prolongation of eosinophi

150 Ras, we show here that activation of Ras and F-actin forms two excitable systems that are coupled thr

151 tively inactivates the negative regulator of F-actin generation, Coronin 1A, at the center of the T c

152 F-actin has been shown to be essential for tip growth in

153 ution structure of a small molecule bound to F-actin, highlighting the potential of electron cryomicr

154 F-actin imaging revealed a cytoplasmic meshwork that mig

155 t the same time, all three isoforms bound to F-actin in a Ca(2+)-independent manner, suggesting that

156 risingly Tpm3.1 retains the capacity to bind F-actin in a cooperative manner.

157 rface of actin and, therefore, interact with F-actin in a mutually exclusive fashion.

158 of ASAP1 reduced colocalization of NM2A and F-actin in cells.

159 lution and that alphaT-catenin monomer binds F-actin in cosedimentation assays as strongly as alphaE-

160 he effects of cross-linking MT plus ends and F-actin in Drosophila melanogaster S2 cells to gain insi

161 F-actin in early stages is consistent with that observed

162 Loss of synaptosomal F-actin in human postmortem tissue correlates directly w

163 ell morphology and disrupted organization of F-actin in Li1 plant cells by confocal microscopy.

164 C into adjacent restricted regions increased F-actin in microvessels in the thrombin-treated and adja

165 ZASP-GFP, a Z-line protein, colocalizes with F-actin in puncta at the cytoplasmic face of nuclei befo

166 ivation in the back/side of the cell or with F-actin in the front of the cell.

167 ges in ARM, and this is supported by reduced F-actin in the mutants and after pharmacological inhibit

168 ic stem and progenitor cells, with increased F-actin in the structure at the rear of the nucleus.

169 ing actin treadmilling in filamentous actin (F-actin) in a nucleotide-state dependent manner.

170 reveal that polymerized actin cytoskeleton (F-actin) in HeLa cells is disorganized by NHERF1, wherea

171 in vitro using fluorescently labeled DNA and F-actin, in which the ensemble orientation of polarized

172 We determined that the EB1:F-actin interaction is salt sensitive and weak under phy

173 These observations suggest that EB1:F-actin interactions may negatively regulate EB1:MT inte

174 s NT (amino-terminal) domain, which mediates F-actin interactions.

175 We show that F-actin is also involved in secretory granule biogenesis

176 unction, indicating that depolymerization of F-actin is causal and not consequent to decreased spine

177 motility of troponin/tropomyosin-free D292V F-actin is normal, motility is dramatically inhibited af

178 Furthermore, we find that F-actin is not essential for the recruitment of NMII to

179 We found stimulated polymerization of F-actin is not required for Syk recruitment but is progr

180 dherin-mediated coupling of the bacterium to F-actin is not required.

181 uctured illumination microscopy reveals that F-actin is reorganized during the course of frustrated p

182 t necessarily weak binding of tropomyosin to F-actin is required for effective thin filament function

183 opose that the primary function of endosomal F-actin is to control the membrane remodeling that accom

184 e found that the cellular filamentous actin (F-actin) is drastically increased in Rictor KO B cells a

185 w for the first time that filamentous actin (F-actin) is lost selectively from synapses early in the

186 CaMKII inhibited AKAP79/150 association with F-actin; it also facilitated AKAP79/150 removal from spi

187 co-localization of JN immunoreactivity with F-actin (labeled with phalloidin) was observed at the ap

188 DT walls showed prominent filamentous actin (F-actin) labeling reflecting cells in a contracted state

189 , and that CYK-1 inhibits INFT-2 to regulate F-actin levels and EXC-6-promoted outgrowth.

190 causes excessive dDia2 activity, maintaining F-actin levels but blocking pseudopod and bleb formation

191 Further, we observed decreased synaptosomal F-actin levels in postmortem brain from mild cognitive i

192 tractile pulses, lower apical E-cadherin and F-actin levels, and aberrantly mobile Rho-kinase structu

193 ple knockout cells still contain near-normal F-actin levels.

194 iated with CORM-401-dependent suppression of F-actin levels/cellular distribution and fMLP-induced ph

195 res the localized activation of the membrane-F-actin linking protein ezrin.

196 2, and activation of CDC42 results in apolar F-actin localization, leading to defects in adhesion, mi

197 CAR (suppressor of cAMP receptor) diminishes F-actin mainly at the cup rim, being consistent with its

198 and force-stabilized binding of vinculin to F-actin may be a mechanism by which adhesion complexes m

199 cles and the elusive motion of a cytoplasmic F-actin mesh, a known regulator of cytoplasmic flows.

200 mplex and above the cuticular plate, a dense F-actin meshwork located underneath the apical plasma me

201 e that by increasing the connectivity of the F-actin meshwork, plastin enables the cortex to generate

202 Speed and space values of the F-actin molecular computers are discussed.

203 link exists between vesicles and cytoplasmic F-actin motion, as recently suggested in mouse oocytes.

204 le size did not slow their velocity, and the F-actin moved with the yolk granules.

205 ontractile ring including filamentous actin (F-actin), myosin, and septins and in forming the subsequ

206 tracked the orientation of sparsely labeled F-actin network at the leading edge of migrating human k

207 icked via the endoplasmic reticulum (ER) and F-actin network inside plant cells.

208 the parasite cytosol and labels an extensive F-actin network that connects parasites within the paras

209 ed to the zippering point by a supracellular F-actin network, which includes an actin cable running a

210 ting rapid displacement of Cdc8 from a dense F-actin network.

211 -dependent alteration of the apical cortical F-actin network.

212 relative to the local retrograde flow of the F-actin network.

213 ERM protein moesin supports the formation of F-actin networks on early endosomes.

214 and cortactin are necessary for formation of F-actin networks that mediate endosome biogenesis or mat

215 or TIRF microscopy of in vitro reconstituted F-actin networks, we observed and characterized two dist

216 vity and segregation to functionally diverse F-actin networks.

217 in to MT plus ends and cross-link the MT and F-actin networks.

218 elp define their associations with different F-actin networks.

219 d that, whereas annexinA2 and ARP2/3 mediate F-actin nucleation and branching, respectively, the ERM

220 lains how Rab11 vesicles support coordinated F-actin nucleation and myosin force generation for vesic

221 e describe the interaction of myosin-5B with F-actin, nucleotides, and the pyrazolopyrimidine compoun

222 Pharmacologic inhibition of F-actin or laser ablation of the cable causes neural fol

223 on experiments indicate that EB1 can bind to F-actin or MTs but not both simultaneously.

224 th this, we found no change in the levels of f-actin or myosin-II at the division plane when CYK-4 GA

225 However, because contractility and F-actin organization are interconnected cytoskeletal pro

226 were found to be mediated by a disruption of F-actin organization that was induced by changes in the

227 f tension-bearing adherens junction (AJ) and F-actin organization to allow formation of an apical TJ

228 ) mutant exhibits defects in endocytosis and F-actin organization, appressorium turgor pressure gener

229 ne dynamics, cell-matrix adhesion status and F-actin organization, this toolbox here enables the dete

230 ive elongation invariably contained a bright F-actin patch at the tip, whereas actin-depleted neurite

231 n is consistent with aura function promoting F-actin polymerization and/or stabilization.

232 is setting established that RHAMM stabilized F-actin polymerization by controlling ROCK signaling.

233 trated that N-WASP is required for localized F-actin polymerization, GLUT4 vesicle translocation, and

234 -dependent, Abl/Src tyrosine kinase-mediated F-actin polymerization.

235 ntenance of total actin levels and preserves F-actin polymerization.

236 ctile myosin-II activity and not to elevated F-actin polymerization.

237 Cortical F-actin prior to furrow formation fails to exhibit a nor

238 n of the TJ-associated ZO-1 and cytoskeletal-F-actin proteins, correlated with modulation of hepatic

239 Imaging of arteries from LifeAct mice showed F-actin rarefaction in the midcellular portion of VSM.

240 microscopy to analyze nuclear morphology and F-actin rearrangements during the initiation, progressio

241 JNK activity was critical for ICAM-1-induced F-actin rearrangements.

242 rypt stem cells resulted in loss of cortical F-actin, reduced cell-cell adhesion, and disrupted local

243 vated fourfold, suggesting an abnormality in F-actin regulation.

244 nd molecular details of its interaction with F-actin remain unclear.

245 id-beta insult caused cofilin activation and F-actin remodeling and decreased microtubule dynamics in

246 g microtubule networks while also regulating F-actin remodeling at the cell rear to promote somal tra

247 Here we identify that Cofilin/ADF-family F-actin remodeling proteins are essential for normal nuc

248 a membrane of skeletal muscle cells requires F-actin remodeling.

249 ptors promote insulin granule exocytosis via F-actin reorganization.

250 egulator branching activity, the increase in F-actin resulting from slowing of actin disassembly, and

251 nts likely disrupts processive elongation of F-actin, resulting in a disorganized cytoskeleton and re

252 xperimentally by comparing cell traction and F-actin retrograde flow for two cell types with differin

253 f U251 glioma cell migration, morphology and F-actin retrograde flow rate can be shifted to lower sti

254 "clutch" myosin-II-based filamentous actin (F-actin) retrograde flow (RF) to promote leading edge me

255 on fails to exhibit a normal transition into F-actin-rich arcs, and drug inhibition is consistent wit

256 domain, massively promoted the formation of F-actin-rich membrane ruffles of COS-7 cells and of dend

257 Comparison to the myosin IIC-F-actin rigor complex reveals an almost complete lack of

258 e did not consistently identify a continuous F-actin ring at the cell surface constriction in mouse e

259 ant, multinucleated TRAP(+) cells capable of F-actin ring formation.

260 the nano-organization of outwardly radiating F-actin rods in cortical neurons from APPswe/PS1DeltaE9

261 84 subunits/s) disassembly, which depends on F-actin's nucleotide-bound state.

262 that cocaine induces alterations in nuclear F-actin signaling pathways in the NAc with associated ch

263 F-actin sliding on human fetal cardiac myosin-coated sur

264 d the overall level of cellular filamentous (F) actin, slowed EC migration and proliferation, and inh

265 ly partially exposes myosin binding sites on F-actin so that binding of rigor myosin is required to f

266 Rather, regulation of F-actin stability by tropomyosin requires fidelity of in

267 e tubulation, endocytosis, and, uniquely, in F-actin stability.

268 These data indicate that F-actin stabilization and Src kinase inhibition represen

269 stored by treatment of ChAc neurons with the F-actin stabilizer phallacidin and the Src kinase inhibi

270 tometry, ELISA of cultured supernatants, and F-actin staining; apoptosis and efferocytosis by morphol

271 There was also loss of wide F-actin stress fibers and large focal adhesions.

272 ependent cation/Ca(2+) influx, thickening of F-actin stress fibers and reinforcement of focal adhesio

273 lamellipodia formation and reorganization of F-actin stress fibers.

274 nts by recognizing time-dependent changes in F-actin structure associated with the hydrolysis of ATP

275 oth mouse and human erythroblasts contain an F-actin structure at the rear of the translocating nucle

276 ation initiates the formation of contractile F-actin structures that surround emigrating neutrophils.

277 nally, competition between Fim1 and Adf1 for F-actin synergizes their activities, promoting rapid dis

278 l model shows that the coupled excitable Ras/F-actin system forms the driving heart for the ordered-s

279 ived patches of activated Ras and associated F-actin that precede the extension of protrusions.

280 thest from the membrane (160-350 nm) we find F-actin, the motor domains of myosins, and a major F-act

281 nistically, we find that by interacting with F-actin, the Par complex and ZO-1, Alix ensures the form

282 In the absence of F-actin, the sperm DNA, centrioles, and organelles were

283 the importance of anchoring the bacterium to F-actin through E-cadherin for bacterial invasion has no

284 ulin forms a force-dependent catch bond with F-actin through its tail domain, but with lifetimes that

285 lood-testis barrier (BTB), co-localized with F-actin, TJ proteins occludin/ZO-1 and basal ES (ectopla

286 We then depolymerized F-actin to decouple vesicle diffusion from actin-mediate

287 tead, sperm contents connect to the cortical F-actin to prevent interaction with the meiotic spindle.

288 myosin 1b cooperates with Arp2/3 to recruit F-actin to the Golgi region where secretory granules bud

289 Energy landscapes based on F-actin-tropomyosin models show the mutation localizes t

290 exploiting the fact that depolymerization of F-actin unleashes SVs focused at the apex by myosin-5 to

291 We found that fibroblasts stained for f-actin using phalloidin conjugated with common fluoroph

292 TP turnover kinetics and their activation by F-actin vary greatly between myosin-2 isoforms.

293 Whereas F-actin, vinculin, and phosphorylated myosin light chain

294 the thrombin-induced increase in endothelial F-actin was determined using confocal fluorescence micro

295 Neutrophil F-actin was elevated fourfold, suggesting an abnormality

296 Increased F-actin was evident in microvessels directly treated wit

297 nt or ring away from the cell periphery, and F-actin was found in podosome-like structures.

298 s tropomyosin blocks myosin binding sites on F-actin, whereas at activating (high-Ca(2+)) conditions

299 ies on the interaction of myosin motors with F-actin, which is regulated through a translocation of t

300 enin.alphaT-catenin heterocomplex also binds F-actin with high affinity unlike the beta-catenin.alpha