ライフサイエンスコーパス: F-actin

1 bind, slide, and cross-link actin filaments (F-actin).

2 ex structure of CPEB3 and an actin filament (F-actin).

3 ncovers or blocks myosin binding sites along F-actin.

4 ns on trailing barbed ends of fascin-bundled F-actin.

5 onal changes in alphaE-catenin when bound to F-actin.

6 ophages, associated with altered pseudopodal F-actin.

7 inal N-BAR domain of ASAP1 directly binds to F-actin.

8 to increase as well as decrease affinity for F-actin.

9 in superhelices as they "lose their grip" on F-actin.

10 enin, which connects the cadherin complex to F-actin.

11 l switching to cooperatively propagate along F-actin.

12 color, fixed plane and volumetric imaging of F-actin.

13 downstream of ABA but upstream of Ca(2+) and F-actin.

14 d bonded tropomyosin alone or tropomyosin on F-actin.

15 myosin that moves on tracks of filamentous (F-) actin.

16 gration and for maintaining normal levels of F-actin [8-10].

17 dexamethasone downregulated LIMK expression, F-actin accumulation at the immune synapse, lytic granul

18 lization of the scaffolding protein Tks5 and F-actin accumulation, followed by later recruitment of S

19 monstrate a surprising role for shuttling of F-actin across cells for lamellipodial expansion.

20 At the same time, host cell F-actin aggregated to form a globular-shaped plug beneat

21 odocytes exhibited more spatially correlated F-actin alignment and a higher rate of detachment under

22 hat substrate stiffness-induced promotion of F-actin alignment occurs concomitantly with a flattened,

23 fibrotic morphology associated with stronger F-actin alignment, SRF and TEAD are up-regulated.

24 and immunofluorescence staining to evaluate F-actin alignment.

25 pes (for example, lack of nuclear shrinkage, F-actin alterations or increased LDH activity); we hypot

26 pm) that promote its binding to filamentous (F)-actin and bias Tpm to an azimuthal location where it

27 had restricted the characterisation of both F-actin and actin regulatory proteins, a limitation we r

28 ofold decrease in tropomyosin's affinity for F-actin and affects leiomodin's function.

29 ling phenocopied the pax2a(-/-) vasculature, F-actin and BM degradation phenotypes.

30 the epithelial basal domain, regulating both F-actin and BM.

31 Arp3), ultimately leading to accumulation of F-actin and Drp1 on the mitochondria.

32 Both proteins bind to F-actin and each other, providing a foundation for netwo

33 te that CCL2 mediates ALIX mobilization from F-actin and enhances HIV-1 release and fitness.

34 -kinase (PI3K) inhibition results in loss of F-actin and expansion of apical-basal domains, which com

35 somes, driving local hyper-polymerization of F-actin and impairing trafficking of the endocytic LRP2

36 on and Cytoskeleton complex, associates with F-actin and is, along with its putative paralog SINE2, e

37 KB) subunit of the CPC caused disassembly of F-actin and keratin between asters and local softening o

38 es and caused AURKB-dependent disassembly of F-actin and keratin that propagated ~40 mum without micr

39 iplakin, plakin family cytolinkers that bind F-actin and keratins, localized to microridges, and were

40 also disruptive cytoskeletal organization of F-actin and MTs through changes in spatial expression of

41 terized by uropod formation, accumulation of F-actin and myosin L chain at the leading edge, and accu

42 sorganization of the cytoskeleton components F-actin and pMLC2.

43 that Angiomotin (AMOT), which can bind both F-actin and the neurosuppressive transcriptional coactiv

44 cleation promoting factor), excess endosomal F-actin and trapping of internalized receptors.

45 iven by the contraction of a ring containing F-actin and type-II myosin.

46 ar how interactions between actin filaments (F-actin) and associated proteins are mechanically regula

47 simultaneously regulates filamentous actin (F-actin) and mTORC2 signaling to achieve equipoise in im

48 Vt binds actin filaments (F-actin) and promotes vinculin dimerization to bundle F-

49 ty of ExoY is stimulated by actin filaments (F-actin) and that ExoY alters actin cytoskeleton dynamic

50 and B-cell lymphopenia, increased neutrophil F-actin, and excessive superoxide production seen in pat

51 ansition of monomeric G-actin to filamentous F-actin, and that several of these effects were differen

52 responsible for generating distinct cortical F-actin architectures and that depletion of either nucle

53 hosphorylation, localization, and binding to F-actin are highly dynamic and dependent on local cytosk

54 Actin filaments (F-actin) are key components of sarcomeres, the basic con

55 In contrast, whether actin filaments (F-actin) are required for or are even present in mitotic

56 complex also influences Tpm's position along F-actin as a function of Ca(2+) to regulate exposure of

57 chloroplast was delayed in the cells lacking F-actin; as this organelle lies directly in the path of

58 to weakly induce the formation of disordered F-actin assemblies.

59 antagonistic relationship between endosomal F-actin assembly and cortical actin bundle integrity dur

60 ological ligands and calcium promote nuclear F-actin assembly for rapid responses towards chromatin d

61 During clathrin-mediated endocytosis, F-actin assembly initiated by the Arp2/3 complex and sev

62 we found that inhibition of Arp2/3-dependent F-actin assembly promotes the reversible relocalization

63 supporting the hypothesis that the defective F-actin assembly results from increased cofilin activity

64 in-coupled receptors (GPCRs) promote nuclear F-actin assembly via heterotrimeric Galpha(q) proteins.

65 P12 suppresses basal Rac and Cdc42 activity, F-actin assembly, invadopodia formation and experimental

66 ments, we attached a phosphorescent probe to F-actin at Cys-374 and performed transient phosphorescen

67 rotrusion through directed polymerization of F-actin at the front.

68 failure is due to inappropriate retention of F-actin at the intercellular bridges between GSC-daughte

69 llipodia and its protrusion coordinated with F-actin at the leading cell edge of live cells.

70 cancer cell lines, resulting in increased in F-actin at the plasma membrane and increased release of

71 ooperate to selectively and rapidly assemble F-actin at the right time and place.

72 shifting azimuthally between three states on F-actin (B-, C-, and M-states) in response to calcium bi

73 develop massively thickened circumferential F-actin bands at their E-cadherin-rich adherens junction

74 a GSK3 inhibitor thinned the circumferential F-actin bands throughout the sensory epithelium of cultu

75 n-rich apical junctions reinforced by robust F-actin bands, and the cells fail to divide.

76 ry of a pharmacological treatment that thins F-actin bands, depletes E-cadherin, and stimulates proli

77 We conducted x-ray crystallography, F-actin binding and bundling assays, and immunofluoresce

78 esized that ExoY oligomerizes in response to F-actin binding and have used the ExoY structure to cons

79 modulating F-actin, while mutants disrupting F-actin binding are defective in its tumorigenic capabil

80 This establishes direct force-activated F-actin binding as a mechanosensing mechanism by which c

81 LIM domain of these proteins disrupt tensed F-actin binding in vitro and cytoskeletal localization i

82 Deleting the AMD increases F-actin binding in vitro and leads to excess actin recru

83 F-actin binding is mediated by the "linker" domain of Ho

84 ictyostelium) and the Cdc42-GEF FGD1-related F-actin binding protein (Frabin) (in human cells).

85 enin's C-terminus eliminates force-activated F-actin binding, and addition of this motif to vinculin

86 F-actin, thus likely outcompeting myosin for F-actin binding.

87 icate that the C-terminal filamentous actin (F-actin)-binding domains are responsible for Tarp-mediat

88 c evidence for the critical role of the Tarp F-actin-binding domains in host cell invasion and for th

89 dity, reducing conformational flexibility of F-actin-binding domains via interdomain cross-talk and c

90 hereas the inositol phospholipid-binding and F-actin-binding domains were essential.

91 gene, is a large sarcolemmal myosin II- and F-actin-binding protein.

92 ic network of actin filaments and associated F-actin-binding proteins, is fundamentally important in

93 he cryo-electron microscopy structure of the F-actin-bound alphaE-catenin actin-binding domain, which

94 alpha-Actinins are major F-actin bundlers that are inhibited by Ca(2+) in nonmusc

95 We used automated image analysis to identify F-actin bundles and crossover junctions and developed a

96 oss-linking, which enables the generation of F-actin bundles required for the sustained stabilization

97 Notably, they fail to inhibit Vt-mediated F-actin bundling and instead promote formation of large

98 te the actin cytoskeleton both directly, via F-actin bundling, and indirectly, via actin-activated nu

99 own that fascin phosphorylation can regulate F-actin bundling, and that this modification can contrib

100 interface plays a crucial role in mediating F-actin bundling.

101 ExoY enzymatic activity was not required for F-actin bundling.

102 omain cross-talk and consequently inhibiting F-actin bundling.

103 Fascin is an F-actin-bundling protein that plays a key role in stabil

104 th high affinity, comparable with eukaryotic F-actin-bundling proteins, such as fimbrin.

105 main of CaMKII may bind either calmodulin or F-actin, but not both.

106 modulation of myosin cross-bridge binding to F-actin by the thin filament troponin (Tn)-tropomyosin (

107 ically prevents dimerization and bundling of F-actin by Vt.

108 ing proteins that stabilize actin filaments (F-actin) by inhibiting actin polymerization and depolyme

109 r studies establish that piconewton force on F-actin can enhance partner binding, which we propose me

110 cy alters the subcellular distribution of an F-actin capping protein in the testis, supporting a role

111 CAPZA2 encodes a subunit of an F-actin-capping protein complex (CapZ).

112 of cytological signatures, including nuclear F-actin cell phenotypes, for classifying the entire spec

113 the distribution and organization of spindle F-actin changes over the course of the cell cycle.

114 We combined filamentous actin (F-actin) chromobodies with gene disruption to assign spe

115 This was associated with impaired F-actin clearing from the center of the cellular interfa

116 ing ionomycin-induced mitochondrial fission, F-actin clouds colocalize with mitochondrial constrictio

117 We performed F-actin co-sedimentation and negative-stain EM experimen

118 a dimer-based structural model for the ExoY-F-actin complex.

119 Unlike the total F-actin concentration, which was high in the front of mi

120 Monomers in the F-actin configuration bound to both barbed and pointed e

121 propose that tandem LIM domains recognize an F-actin conformation that is rare in the relaxed state b

122 ssociated with the furrows in the absence of F-actin, consistent with the possibility that the microt

123 into myofibroblasts but normal migration and F-actin content, most likely as a result of compensatory

124 functions at postsynaptic sites to modulate F-actin control by RhoA and regulate synapse maintenance

125 F-actin could be chemically modulated, and genetically d

126 r activity, in the form of ATP hydrolysis on F-actin coupled to nucleotide-dependent cofilin binding,

127 ects these functions through SEPT9-dependent F-actin cross-linking, which enables the generation of F

128 inker length is not a primary determinant of F-actin cross-linking.

129 Conoidal FRM1 initiates a flux of F-actin crucial for motility, invasion and egress.

130 We also find that there is an "F-actin cycle," in which the distribution and organizati

131 veals distinct regulatory mechanisms control F-actin cytoskeletal and/or membrane maintenance in post

132 on via their effects on microtubule (MT) and F-actin cytoskeletal organization across the epithelium.

133 organ of Corti and much lower expression of F-actin cytoskeleton in the cochlea compared with wild-t

134 ator of mesenchymal cell adhesion signaling, F-actin cytoskeleton remodeling and single cell migratio

135 ts was associated with the disruption of the F-actin cytoskeleton.

136 irement in the recruitment of the ring canal F-actin cytoskeleton.

137 Our data describe an F-actin dependent mechanism in apicomplexans for transpo

138 While this recycling pathway is F-actin dependent, de novo synthesis of micronemes appea

139 the phosphorylation and inactivation of the F-actin depolymerization factor cofilin to induce TNT fo

140 ic level, Sema3E/PlexinD1 signaling promoted F-actin disassembly and focal adhesion reduction by acti

141 SEMA3F-mediated retention is associated with F-actin disassembly.

142 Here, we address the mechanism of F-actin-driven NE rupture by correlated live-cell, super

143 Here, we show that YAP co-localizes with F-actin during activating conditions, such as sparse pla

144 ted cerebellar neurons dramatically affected F-actin dynamics and reduced neurite outgrowth, which ha

145 l dendrite patterning by directly modulating F-actin dynamics through TIAM-1/GEF.

146 ein that regulates microtubule stability and F-actin dynamics.

147 of cofilin, Wdr1, and coronin in regulating F-actin dynamics.

148 he inability to visualise filamentous actin (F-actin) dynamics had restricted the characterisation of

149 e tools for live imaging of actin filaments (F-actin) enabled the detection of surprising nuclear str

150 Microtubules and filamentous (F-) actin engage in complex interactions to drive many c

151 w single piconewton forces applied solely to F-actin enhance binding by the human version of the esse

152 st actin binding proteins (ABPs) for binding F-actin facilitates their sorting to different cellular

153 complex-mediated cell-autonomous control of F-actin fiber orientation relies on the preceding BM fib

154 in FHOD1 and INF2-mediated unbranched radial F-actin fibers emanating from invadopodia and rosettes,

155 ng of capsular bags for the fibrotic markers f-actin, fibronectin, alpha smooth muscle actin, and col

156 The fibrotic markers f-actin, fibronectin, alpha smooth muscle actin, and col

157 d to both barbed and pointed ends of a short F-actin filament at the anticipated locations for polyme

158 gle CaMKII holoenzymes cross-linked multiple F-actin filaments at random, whereas at higher CaMKII/F-

159 monomeric G-actin but increased filamentous F-actin following CD44 RNAi suggested a possible role fo

160 Simulations with multiple monomers in the F-actin form show assembly into filaments as well as tra

161 Finally, we mapped subapical F-actin fringe and trans-Golgi network positioning relat

162 crovilli; it also led to a redistribution of F-actin from cortical lateral networks into the brush bo

163 omponents at the nuclear envelope, increased F-actin/G-actin ratios, and deregulation of mechanorespo

164 d mechanical load strengthens its binding to F-actin in a direction-sensitive manner.

165 te features that affect CH1-CH2 affinity for F-actin in cells and in vitro, we perturbed the utrophin

166 we conclude that there is far more internal F-actin in epithelial cells than is commonly believed.

167 used as the "recognition unit" (ligand) for F-actin in living cells.

168 We found that ASAP1 homodimerization aligns F-actin in predominantly unipolar bundles and stabilizes

169 umen can be occupied by extended segments of F-actin in small molecule-induced, microtubule-based, ce

170 e we show that after initial cell spreading, F-actin in synapses of primary mouse B cells and human B

171 understood and has been proposed to rely on F-actin in the bridge region.

172 ated endocytosis, macropinosomes encapsulate F-actin in the cell body, forming vesicles that transloc

173 Finally, we find that binding to tensed F-actin in the cytoplasm excludes the cancer-associated

174 olled by higher cofilin-mediated turnover of F-actin in the front.

175 d that pax2a(-/-) embryos fail to accumulate F-actin in the OF prior to basement membrane (BM) degrad

176 increased binding and bundling activity with F-actin in vitro.

177 etion of GOLPH3 alone or depolymerization of F-actin in WASp-sufficient T(H) cells still allows devel

178 e novo synthesis of micronemes appears to be F-actin independent.

179 We also propose that the CPEB3/F-actin interaction might be regulated by the SUMOylatio

180 Our model of the CPEB3/F-actin interaction suggests that F-actin potentially tr

181 To address this, we characterized the F-actin interactome in spread interphase and round mitot

182 and promotes vinculin dimerization to bundle F-actin into thick fibers.

183 mydomonas reinhardtii We found that although F-actin is associated with the furrow region, none of th

184 fically enriched in active protrusions where F-actin is devoid of non-muscle myosin II activity.

185 Branched F-actin is generated by the nucleation factor actin-rela

186 ild-type and mutant tropomyosin molecules on F-actin, is not complicated by tropomyosin polymerizatio

187 rate that Formin-2, a predicted nucleator of F-actin, is responsible for apicoplast inheritance in bo

188 culum (ER), mitochondria, acidic organelles, F-actin, keratin, and soluble fluorescein.

189 Conversely, overexpressing EB1 decreases F-actin levels and impairs directed cell migration witho

190 Consistently, in MsrB2-depleted cells, F-actin levels are decreased in ICBs, and dividing cells

191 substrate, cortactin, resulting in increased F-actin levels at the plasma membrane.

192 on cell-substratum adhesion and cytoskeletal F-actin levels based on nutrient availability, and these

193 al observations, knocking down EB1 increases F-actin levels in cells, and this can be rescued by disr

194 CYK-1 is critical for normal F-actin levels in the contractile ring, and acute inhibi

195 Loss of LUZP1 reduces F-actin levels, facilitates ciliogenesis and alters Soni

196 assembly is critical for maintaining normal F-actin levels, organization, and dynamics at FAs, along

197 epletion correlating with the time course of F-actin loss.

198 Successive reorganization of an F-actin meshwork, associated with microtubular structure

199 the cytoskeleton including actin filaments (F-actin), microtubules (MT), and intermediate filaments

200 s the PM PI(4,5)P(2) coincident with altered F-actin morphology, and reduces both VEGFR2 and choleste

201 changes in the density of membrane-proximal F-actin (MPA) during membrane protrusion and cell migrat

202 ntractile actomyosin ring (AMR), composed of F-actin, myosin II, and other actin and myosin II regula

203 of how force generation can be controlled by F-actin-myosin interactions.

204 The F-actin network connects individual parasites, supports

205 trusion and provide localized ATP that fuels F-actin network growth.

206 conclude that there is a robust endoplasmic F-actin network in normal vertebrate epithelial cells an

207 Since a distinct F-actin network resides precisely at the site of disc mo

208 nockout resulted in the complete loss of the F-actin network specifically at the site of disc morphog

209 hat a dorsal-ventral polarized supracellular F-actin network, running around the egg chamber on the b

210 ng daughter parasites using a highly dynamic F-actin network.

211 and are collapsed due to changes within the F-actin network.

212 h leads to remodeling of the actin filament (F-actin) network in the spine.

213 NLR-1 can directly bind to actin to recruit F-actin networks at the gap junction formation plaque, a

214 on yeast Pxl1 binds to mechanically stressed F-actin networks but does not associate with relaxed act

215 elongation factors that localize to diverse F-actin networks composed of filaments bundled by differ

216 tivity to balance the endosomal and cortical F-actin networks during epithelial tube maturation.

217 ABPs) sort to different regions to establish F-actin networks with diverse functions, including filop

218 standing the mechanics of more physiological F-actin networks with turnover and inform an updated mic

219 gap junction formation through anchoring of F-actin networks.

220 apable of inhibiting Fim1's association with F-actin networks.

221 ine-phalloidin stabilized filamentous actin (F-actin) networks cross-linked by CaMKII.

222 ated assembly of multiple filamentous actin (F-actin) networks from an actin monomer pool is importan

223 However, F-actin next to the plasma membrane also tethers the mem

224 1A, fully restores the cortical location of F-actin, nuclear integrity, viability, and mobility of W

225 d actin assembly by strongly inhibiting both F-actin nucleation and barbed-end elongation at equimola

226 1 and the ARP2/3 complex are the predominant F-actin nucleators responsible for generating distinct c

227 Cyclophilin A localizes within the F-actin of these structures and is crucial for their pro

228 ntatives of all three families directly bind F-actin only in the presence of mechanical force.

229 Unlike F-actin or microtubules, keratins are the first major co

230 exchange factor (GEF) Ect2 to control local F-actin organization and contractility in this subcellul

231 ction formation plaque, and the formation of F-actin patches plays a critical role in the assembly of

232 d polymerization, G-actin did not bind at an F-actin pointed end.

233 cium and inhibition of the Arp2/3 complex or F-actin polymerization also caused a decrease in the abi

234 ent of the abscission checkpoint that favors F-actin polymerization and limits tetraploidy, a startin

235 to connect phosphatidylinositol signaling to F-actin polymerization at the podosome.

236 g to the nuclear periphery driven by nuclear F-actin polymerization in cells with POT1 mutations.

237 phosphate lipid (PI(3,4,5)P3) production and F-actin polymerization take place at integrin-mediated a

238 cells promoted cell migration and decreased F-actin polymerization, while overexpression of ASB13 su

239 While F-actin polymerizations are initialized from the ventral

240 Further, we identify an F-actin population - stable base clusters - that orchest

241 the CPEB3/F-actin interaction suggests that F-actin potentially triggers the aggregation-prone struc

242 ilaments at random, whereas at higher CaMKII/F-actin ratios, filaments bundled.

243 light the different spatial requirements for F-actin regulation in Toxoplasma which appear to be achi

244 art, attributed to impairments in Ca(2+) and F-actin regulation.

245 uggest that subtle disturbances of postnatal F-actin remodeling are sufficient for predisposing muscl

246 LIM kinase (LIMK) regulates F-actin remodeling by phosphorylating cofilin to inhibit

247 nhancement of p38 MAPK signaling, leading to F-actin reorganization and activation of nuclear factor

248 to increased H(2)O(2) and Ca(2+) levels and F-actin reorganization, but the mechanism of, and connec

249 with F-actin, which is dependent upon their F-actin residence time.

250 roscopy structures of both proteins bound to F-actin reveal unique rearrangements that facilitate the

251 xonal GCs, preventing MT depolymerization in F-actin-rich areas.

252 recruited at sites of phagosome formation in F-actin-rich cups.

253 NAV1 accumulates in F-actin-rich domains of GCs and binds actin filaments in

254 cell membrane, which drives formation of an F-actin-rich protrusion that physically breaches and dis

255 Filopodia are peripheral F-actin-rich structures that enable cell sensing of the

256 ls reveals defects in the filamentous actin (F-actin)-scaffolded acroplaxome during spermatid elongat

257 to myosin motor activity leading to enhanced F-actin severing of possible physiological relevance.

258 alized NE is mediated by an Arp2/3-nucleated F-actin 'shell' in starfish oocytes, in contrast to micr

259 etch revealed similar divergent trends, with F-actin shifting away from (5% strain) or toward (20% st

260 endent protein kinase (DNA-PK)-myosin XVIIIA-F-actin signaling pathway.

261 , a thin network of dynamic actin filaments (F-actin) situated just beneath the plasma membrane.

262 site staining of SA along with the competing F-actin specific fluorescent conjugate, phalloidin, and

263 These F-actin spikes protrude pore-free nuclear membranes, whe

264 t-dependent effectors were designed from the F-actin-stabilizing marine depsipeptide jasplakinolide b

265 Squamous cells with nuclear F-actin staining were associated with early disease (i.e

266 VEGF-induced endothelial cell signaling for F-actin stress fiber inducing endothelial barrier dysfun

267 ies show that YAP activation is dependent on F-actin stress fiber mediated nuclear pore opening, howe

268 esion molecules was accompanied by increased F-actin stress fibers and increased endothelial barrier

269 oriented basement membrane (BM) fibrils and F-actin stress fibers constrain follicle growth, promoti

270 estinal epithelial tight junction and within F-actin stress fibers where it is critical for barrier i

271 e that HIPK4 overexpression induces branched F-actin structures in cultured fibroblasts and that HIPK

272 CCL2 immuno-depletion sequestered ALIX to F-actin structures, while CCL2 addition mobilized it to

273 Study of filamentous-actin (F-actin) subsequently showed that SEMA3F-mediated retent

274 s and continuous tropomyosin cables over the F-actin substrate, which were optimized further by flexi

275 Computational models of MVt bound to F-actin suggest that MVt undergoes a conformational chan

276 cal analysis demonstrated that Spindly binds F-actin, suggesting that Spindly serves as a link betwee

277 atenin's C-terminus is a modular detector of F-actin tension.

278 mostly unphosphorylated and associated with F-actin, thus likely outcompeting myosin for F-actin bin

279 hich highlight the surface feature's role in F-actin-Tm interactions and contractile regulation.

280 spectrin is required for tethering cortical F-actin to cell membrane domains outside the adherens ju

281 s head to tail along the long-pitch helix of F-actin to form continuous superhelical cables that wrap

282 pectrin, the weakened attachment of cortical F-actin to plasma membrane results in a failure to trans

283 er 4 degrees dendrite branches by localizing F-actin to the distal ends of developing dendrites.

284 n acetylation did not disrupt characteristic F-actin-Tpm binding.

285 myosin attachment, as reflected by increased F-actin-Tpm motility that persisted in the presence of T

286 nd Lys(328), also resulted in less inhibited F-actin-Tpm, implying that modifying only these residues

287 Release of CaMKII from F-actin, triggered by calcium-calmodulin, was too rapid

288 modulate acto-myosin activity by optimizing F-actin-tropomyosin interfacial contacts and by binding

289 TNT1's propensity to inhibit myosin-driven, F-actin-tropomyosin motility were evaluated.

290 oscopy reconstruction of myosin-S1-decorated F-actin-tropomyosin together with atomic scale protein-p

291 ructures, possibly through direct binding to F-actin via its N-BAR domain.

292 Moreover, when F-actin was eliminated through a combination of a mutati

293 Since SP stabilizes F-actin, we speculated that the presence of SP within la

294 ted over potential "target" binding sites on F-actin where the corresponding interaction energetics o

295 hor tropomyosin to an inhibitory position on F-actin, where it deters myosin binding at rest, and tha

296 Fim1 competes with Ain1 for association with F-actin, which is dependent upon their F-actin residence

297 egulates the cytoskeleton through modulating F-actin, while mutants disrupting F-actin binding are de

298 pha with a polyclonal antibody and host cell F-actin with rhodamine-phalloidin.

299 We observe the co-segregation of copper and F-actin within the nano-architecture of dendritic protru

300 s the turnover and spatial reorganization of F-actin, without significant changes to filament length.