ライフサイエンスコーパス: G-actin

1 -actin) but not to globular monomeric actin (G-actin).

2 ch will increase the pool of globular actin (G-actin).

3 ence of high concentrations of polymerizable G actin.

4 erize actin in the presence of polymerizable G actin.

5 inetics of seven actin-binding proteins with G-actin.

6 med by the seven actin-binding proteins with G-actin.

7 and has been shown to covalently cross-link G-actin.

8 MRTF-A RPEL domain occurs competitively with G-actin.

9 ort pathway, and that import is inhibited by G-actin.

10 olymerization by Bnr1 does not occur with Ca-G-actin.

11 o not affect the interaction of cofilin with G-actin.

12 ite complex additionally involving Cap1p and G-actin.

13 for the HIV-1 CA protein dimer and ATP-bound G-actin.

14 n dynamics, which alter its interaction with G-actin.

15 inal segment of cofilin in interactions with G-actin.

16 e in R(2) compared to unpolymerized ferritin-G-actin.

17 ysteines in the regions predicted to bind to G-actin.

18 ll likely have increased levels of monomeric G-actin.

19 is involved in a weak binding of cofilin to G-actin.

20 C-terminal and N-terminal halves+/-monomeric G-actin.

21 tin, with a broader distance distribution in G-actin.

22 site corresponds to one of the subdomains of G-actin.

23 time, in vitro re-folding of EDTA-denatured G-actin.

24 roups were selectively labeled to Cys-374 on G-actin.

25 ndance of activated Arp2/3 and polymerizable G-actin.

26 tin filament was reconstituted from purified G-actin.

27 PPP1R15-PP1 phosphatase identified monomeric G-actin.

28 ent-like (F-actin) conformation in ATP-bound G-actin.

29 eractions between different MC states within G-actin (6 kcal/mol) is similar to that found for comple

30 Local microinjection of Myo1c promoted G-actin accumulation and plasma membrane ruffling, and M

31 These data, along with changes in G-actin accumulation in the oocyte nucleus, suggest that

32 dmill, which in turn depends on recycling of G-actin across the cell, from the rear where F-actin dis

33 elerate F-actin depolymerization and provide G-actin, alone or in complex with actin-binding proteins

34 We found that the concentration profile of G actin along the filopodium is rather nontrivial, conta

35 hosphorylation resulted in increased nuclear G actin and phosphorylated actin.

36 cytoskeleton by inhibiting polymerization of G-actin and disrupting the formation of stress fibers.

37 rofilins are of key interest as they bind to G-actin and enhance actin polymerization.

38 Here we review structures of G-actin and F-actin and discuss some of the interactions

39 different roles, we directly compared their G-actin and F-actin binding affinities, and quantified t

40 One is analogous to the G-actin and F-actin binding site on cofilin, but we show

41 hree ADF/Cofilins had similar affinities for G-actin and F-actin.

42 ires profilin and its interactions with both G-actin and formins.

43 that uncouple its interactions with Bni1 and G-actin and found that both interactions are critical fo

44 ly due to the reduced binding of MRTF-A/B to G-actin and in part, to the low level of MRTF-A phosphor

45 s gene expression pattern and showed reduced G-actin and increased nuclear localization of MKL1, each

46 on of nuclear actin, which decreases nuclear G-actin and increases MRTF-A in the nucleus.

47 l) is similar to that found for complexes of G-actin and its regulatory proteins.

48 uences, structural folds, and affinities for G-actin and poly-L-proline, budding yeast profilin ScPFY

49 ocalized to the cytosol, divided between the G-actin and short filamentous actin (sF-actin) fractions

50 diffusion of water in F-actin as compared to G-actin and shorter water wires between Asp154 and the n

51 S3A cofilin mutant resulted in a decrease of G-actin and the actin stress fiber formation, the effect

52 e coil-to-helix transition of the DB-loop in G-actin and the open-to-closed transition of adenylate k

53 signaling, which alters interactions between G-actin and the RPEL domain.

54 ively with excess Arp2/3 complex for limited G-actin and to assemble F-actin for contractile ring for

55 this required interactions of profilin with G-actin and VASP.

56 tions and TJs readily incorporated exogenous G-actin and were disassembled by latrunculin B, thus ind

57 its ability to transition between monomeric (G-actin) and filamentous (F-actin) states under the cont

58 protein that binds to both monomeric actin (G-actin) and polymeric actin (F-actin) and is involved i

59 ia coli and tested their binding toward TM5, G-actin, and F-actin.

60 G-actin, profilin- and thymosin-beta4-bound G-actin, and free barbed and pointed ends of actin filam

61 The MRTFs bind G-actin, and signal-regulated changes in cellular G-acti

62 uch as the HIV-1 CA protein dimer, ATP-bound G-actin, and the Arp2/3 complex.

63 binding tail domain of Myo1c interacted with G-actin, and the motor domain was required for the trans

64 2) N-ABD binds to F-actin and C-ABD binds to G-actin; and 3) F-actin binding to N-ABD may prevent G-a

65 ility to bind F-actin and profilin-complexed G-actin are important for its effect, whereas Ena/VASP t

66 ough crystal structures for monomeric actin (G-actin) are available, a high-resolution structure of F

67 r determining the extent of stimulus-induced G-actin assembly and cell extension.

68 Like PP1, G-actin associated with the functional core of PPP1R15 f

69 io resulting in nuclear translocation of the G-actin-associated transcriptional cofactor, megakaryobl

70 ls diminished interaction between Tbeta4 and G-actin at the cell leading edge despite their colocaliz

71 tin accompanied by increased globular-actin (G-actin) at as early as 1 month of age in a mouse model

72 Bud6 into a Bni1-binding "core" domain and a G-actin binding "flank" domain.

73 This requires profilin's G-actin binding activity and its direct interaction with

74 cells in vivo by a combination of reversible G-actin binding and effective F-actin severing.

75 hymosin beta4 (Tbeta4) is a highly conserved G-actin binding polypeptide with multiple intra- and ext

76 in assembly factors, we found that the small G-actin binding protein profilin directly inhibits Arp2/

77 n actin-stabilized cells is dependent on the G-actin binding region of the cyclase-associated protein

78 ered at low pH coincide with segments of the G-actin binding surface and poly-l-proline binding inter

79 To model the regulation of G-actin binding to a cell surface receptor we used the c

80 Previous results indicated that G-actin binding to MKL1 promotes its nuclear export, and

81 of the WH2 domain, which is responsible for G-actin binding, enhanced cell motility.

82 We demonstrate that, upon G-actin binding, thymosin ss4 (Tss4), induces MRTF trans

83 reversible availability of this residue for G-actin binding.

84 uires self-association but is independent of G-actin binding.

85 n simultaneously to this poly-Pro and to the G-actin-binding (GAB) domain of VASP.

86 onstrated a critical functional role for the G-actin-binding C-terminal half of Srv2.

87 Mutation of the G-actin-binding motif (GAB) partially compromised stabil

88 Leiomodin (Lmod) is a class of potent tandem-G-actin-binding nucleators in muscle cells.

89 gnal transduction mediated by certain tandem-G-actin-binding nucleators.

90 These activities are independent of the G-actin-binding properties of Tbeta(4).

91 the vitamin-D-binding protein, extending the G-actin-binding protein repertoire.

92 We selected two vital Plasmodium berghei G-actin-binding proteins, C-CAP and profilin, in combina

93 ing sites were detected: a calcium-dependent G-actin-binding site in G1 and a calcium-independent G-

94 ack growing filament barbed ends while three G-actin-binding sites (GABs) on other arms are available

95 ontaining five F-actin-binding sites and two G-actin-binding sites, and interacts with wheat (Triticu

96 nucleator Cobl, despite having only a single G-actin-binding Wiskott-Aldrich syndrome protein Homolog

97 ell adhesion molecule 1 (CEACAM1-S) in which G-actin binds to its short cytoplasmic domain.

98 A liposome model system demonstrates that G-actin binds to the cytosolic domain peptide of CEACAM1

99 nd velocity runs revealed oligomers of AC in G-actin buffer.

100 pressive, < or = 30%, due to sequestering of G-actin by freely diffusing motors.

101 lored the possibility of active transport of G-actin by myosin motors, which would be an expected bio

102 Analytical ultracentrifugation profiles of G-actin can be ascribed to the existence of actin monome

103 fferent photochromes specifically labeled to G-actin can be used to rapidly and reversibly modulate s

104 igomerization and its binding to profilin, a G-actin chaperone.

105 The second class encodes proteins that bind G-actin (COF1, SRV2, and PFY1), indicating that reductio

106 Although an atomic structure of the G-actin-cofilin complex does not exist, models of the co

107 ur results showed greater exchange for yeast G-actin compared with muscle actin in the barbed end piv

108 sm for pH induced disruption of the profilin-G-actin complex involve a nativelike unfolding intermedi

109 The abundance of the ternary PPP1R15-PP1-G-actin complex was responsive to global changes in the

110 ted S98 phosphorylation inhibits assembly of G-actin complexes on the MRTF-A regulatory RPEL domain,

111 uctures of two independent RPEL(MAL) peptide:G-actin complexes.

112 in, and signal-regulated changes in cellular G-actin concentration control their nuclear accumulation

113 e diffusion-drift-reaction equations for the G-actin concentration in a realistic three-dimensional g

114 Multipoint FDAP analysis revealed that G-actin concentration in lamellipodia was comparable to

115 ue for quantifying spatiotemporal changes in G-actin concentration in live cells, consisting of seque

116 To understand the intracellular role of G-actin concentration in stimulus-induced actin assembly

117 and cell extension correlated linearly with G-actin concentration in unstimulated cells, even at con

118 actin filaments, indicating that cytoplasmic G-actin concentration is a critical parameter for determ

119 f jasplakinolide-induced temporal changes in G-actin concentration.

120 ts a dual role for TgADF in maintaining high G-actin concentrations and effecting rapid filament turn

121 Cytoplasmic G-actin concentrations decreased by approximately 40% im

122 comet tails in the presence of physiological G-actin concentrations this mixture was insufficient to

123 Alternate excitation of spirobenzopyran G-actin conjugates with 365 and 546 nm leads to rapid tr

124 The potential energy of a CG G-actin contains three bonds, two angles, and one dihedr

125 Pressurization reduced G-actin content and elevated the levels of cofilin and H

126 significant changes in arterial diameter and G-actin content of myogenically active arteries.

127 A decline in G-actin content was observed following pressurization fr

128 n, caldesmon, cofilin, and HSP27, as well as G-actin content, were determined.

129 sin-beta4 (Tbeta4) binding to actin monomer (G-actin) coordinates actin polymerization with metallopr

130 ate of the receptor, and cellular factors (e.g. actin cytoskeleton and lipid rafts) influence the ass

131 Overexpression of MKL1 or reduction in G-actin decreased insulin-stimulated Akt phosphorylation

132 yo1c knockdown confirmed its contribution to G-actin delivery to the leading edge and for cell motili

133 In this issue, Lei et al. reports a novel, G-actin-dependent regulation of actin polymerization wit

134 rected phosphatase activity, while localised G-actin depletion at sites enriched for PPP1R15 enhanced

135 unctional core of PPP1R15 family members and G-actin depletion, by the marine toxin jasplakinolide, d

136 induced actin polymerisation and concomitant G-actin depletion, MRTFs accumulate in the nucleus and a

137 stigate the effect of steric restrictions on G-actin diffusion by the porous structure of filopodial

138 sistance, lamellipodial protrusion rate, and G-actin diffusion coefficient.

139 As measured by surface plasmon resonance, G-actin directly interacts with PMCA with an apparent 1:

140 treadmill, and we demonstrate that measured G-actin distributions are consistent with the existence

141 with isolated PMCA and examine the effect of G-actin during the first polymerization steps.

142 Here we report that a pool of G-actin dynamically localizes to the leading edge of gro

143 We identify important differences in G-actin engagement between the two RPEL(MAL) structures.

144 Inhibition of GAS DNase activity with G-actin enhanced neutrophil clearance of the pathogen in

145 indicating the importance of maintaining F-/G-actin equilibrium for optimal behavioral response.

146 proach that allows us to monitor F-actin and G-actin equilibrium in living cells through the use of t

147 of the alpha,beta-tubulin-microtubule and/or G-actin-F-actin equilibria.

148 tensile force regulates G-actin/G-actin and G-actin/F-actin dissociation kinetics by prolonging bond

149 MO7 colocalizes with F-actin and reduces the G-actin/F-actin ratio via a Rho-independent mechanism.

150 drophobic loop is mobile in F- as well as in G-actin, fluctuating between the extended and parked con

151 of G-actin monomers, which leads to smaller G-actin flux along the filopodial tube compared with the

152 ay thus modulate the availability of TM5 and G-actin for E-Tmod41 to construct the protofilament-base

153 establish a G-actin gradient that transports G-actin forward "globally" across the lamellipod.

154 and 3) F-actin binding to N-ABD may prevent G-actin from binding to C-ABD.

155 Tbeta4 prevents G-actin from joining a filament, whereas profilin:actin

156 Recent x-ray structures of ADP-bound G-actin (G-ADP) by Otterbein et al. and ATP-bound G-acti

157 in (G-ADP) by Otterbein et al. and ATP-bound G-actin (G-ATP) by Graceffa and Dominguez indicate that

158 iments, we show that tensile force regulates G-actin/G-actin and G-actin/F-actin dissociation kinetic

159 the front, along with diffusion, establish a G-actin gradient that transports G-actin forward "global

160 k created by the membrane load and monomeric G-actin gradient.

161 lin to the subdomain 1/subdomain 3 region on G-actin has been probed using site-directed mutagenesis,

162 n in a cell is critical, and competition for G-actin helps regulate the proper amount of F-actin asse

163 tition for a limited pool of actin monomers (G-actin) helps to regulate their size and density.

164 te the bulk of F-actin from a common pool of G-actin; however, the interplay and/or competition betwe

165 Both RPEL peptides bind to the G-actin hydrophobic cleft and to subdomain 3.

166 s are elevated in spines upon activity, with G-actin immobilized by the local enrichment of phosphati

167 the two WH2 domains in V, VC, and VCA binds G-actin in 1:2 complexes that participate in barbed end

168 tion of actin polymerization to sequestering G-actin in 1ratio1 complexes.

169 for myosin II contractile-based transport of G-actin in ECs.

170 uses the polymerization of pyrene-labeled Mg-G-actin in G-buffer into single filaments based on fluor

171 the dynamic equilibrium between F-actin and G-actin in intact cells.

172 actin mutant, we show vectorial transport of G-actin in live migrating endothelial cells (ECs).

173 vel mechanism by which dynamic enrichment of G-actin in spines regulates the actin remodeling underly

174 dynamic (i.e., do not exchange subunits with G-actin in the cytosol), this assumption has never been

175 was partly the result of an accumulation of G-actin in the salivary placodes, indicating that Tec29

176 utually exclusively to cellular and purified G-actin in vitro The competition by different WH2 domain

177 onformational mobility of the actin monomer (G-actin) in a coarse-grained subspace using umbrella sam

178 spatiotemporal enrichment of actin monomers (G-actin) in dendritic spines regulates spine development

179 determined for the loss of ATP from Ca-free G-actin, in good agreement with previous studies.

180 are stable structures that require constant G-actin incorporation and are distinct from the actin we

181 human VSMCs, stimulation with PDGF increased G-actin incorporation into the actin cytoskeleton.

182 inhibited the rate of nucleotide exchange on G-actin, indicating that AtADF4 is a bona fide actin-dep

183 al F-actin-binding motor protein, as a major G-actin-interacting protein.

184 Characterisation of the RPEL(MAL):G-actin interaction by fluorescence anisotropy and cell

185 n, preventing the incorporation of the bound G-actin into a filament.

186 alyzes a covalent cross-linking of monomeric G-actin into oligomeric chains and causes cell rounding,

187 Global (G)-actin is able to assemble into highly organized, supr

188 However, the mechanism by which G-actin is correctly distributed between rival F-actin n

189 the binding specificity of twinfilin for ADP-G-actin is crucial for the observed biphasic evolution o

190 es C and pressures up to 1 kbar are reached, G-actin is hardly stable.

191 G-actin is not only the least temperature-stable but als

192 In addition, G-actin is proposed as a cytoskeletal substrate of the R

193 ents are stable for long times even when the G-actin is removed from the supernatant-making this a pr

194 Spatial distribution of G-actin is smooth and not sensitive to F-actin density f

195 Each actin monomer (G-actin) is coarse-grained into four sites, and each sit

196 sis, whereby competition for actin monomers (G-actin) is critical for regulating F-actin network size

197 Monomeric globular actin (G-actin) is the building block for F-actin but is not co

198 cross-linking depletes the cellular pool of G-actin leading to actin cytoskeleton depolymerization.

199 actin cross-linking domain (ACD) cross-links G-actin, leading to F-actin depolymerization, cytoskelet

200 response to signal is inhibited by increased G-actin level.

201 Cellular F-actin/G-actin levels also regulate serum response factor (SRF)

202 desartan and PKC inhibition caused increased G-actin levels, as determined by Western blotting of ves

203 L1 nuclear localization due to a decrease in G-actin levels, but MKL1 is then downregulated by nuclea

204 The SRF pathway registers changes in G-actin levels, leading to the transcriptional up-regula

205 rogated through reduction of globular actin (G-actin) levels and disturbed expression of multiple act

206 Loss of G-actin localization leads to the cessation and retracti

207 Moreover, G-actin localization occurs asymmetrically in growth con

208 The extent of stimulus-induced G-actin loss and cell extension correlated linearly with

209 several mRNAs involved in these processes (e.g., Actin, matrix metalloproteinase 9, and cyclin D1 and

210 imers and that the Bud6 flank binds a single G-actin molecule.

211 hought to act by liberating cofilin from ADP.G-actin monomers to restore cofilin activity.

212 ilopodial length is diffusional transport of G-actin monomers to the polymerizing barbed ends.

213 so observed significant diffusional noise of G-actin monomers, which leads to smaller G-actin flux al

214 tin states are compared with those of Mg-ATP-G-actin (monomers) analyzed previously.

215 minal 102 residues, E-Tmod29 binds to TM5 or G-actin more strongly than E-Tmod41 does, but barely bin

216 ally requires the dissociation of repressive G-actin-MRTF-A complexes.

217 cytoskeletal dynamics is its facilitation of G-actin nucleotide exchange.

218 ly; optical switching within spirobenzopyran-G-actin occurs with high fidelity and the recovery of sp

219 for ATP hydrolysis in F-actin as compared to G-actin of 8 +/- 1 kcal/mol, in good agreement with the

220 ng an activation energy for the unfolding of G-actin of 81.3(+/-3.3) kJ mol(-1).

221 erved rate increase over the monomeric form, G-actin, of 4.3 x 10(4).

222 In contrast, SK1 bound G-actin only under stimulated conditions.

223 tobleaching assay, as well as an increase in G-actin polymerization and a decrease in F-actin depolym

224 hosphorylation attenuates MCP1-induced HASMC G-actin polymerization, F-actin stress fiber formation,

225 hosphorylation, cortactin-WAVE2 interaction, G-actin polymerization, F-actin stress fiber formation,

226 cortactin interaction with WAVE2, affecting G-actin polymerization, F-actin stress fiber formation,

227 We further find that this G-actin pool functions in spine development and its modi

228 Mechanistically, the relatively immobile G-actin pool in spines depends on the phosphoinositide P

229 ibers present increased replenishment of the G-actin pool, therefore prolonging Arp2/3-nucleated CDR

230 e expression through control of the cellular G-actin pool.

231 aments against dynamic F-actin and monomeric G-actin populations in live cells, with negligible disru

232 that bind at the barbed and pointed faces of G-actin, preventing the incorporation of the bound G-act

233 assessed the cellular concentrations of free G-actin, profilin- and thymosin-beta4-bound G-actin, and

234 results suggest that dynamic localization of G-actin provides a novel mechanism to regulate the spati

235 polymerization of actin and changes in the F/G actin ratio resulting in nuclear translocation of the

236 actin rearrangement and an increase in the F/G actin ratio.

237 The filamentous (F) to globular (G) actin ratio, known to regulate myocardin family trans

238 th an abnormally low filamentous/globular (F/G)-actin ratio that may be the underlying cause of sever

239 isplay smaller growth cones with a reduced F/G-actin ratio.

240 Furthermore, the increase in F/G-actin ratios (an index of actin assembly) and constric

241 ls of ICAM-1 further reduce TEER, increase F/G-actin ratios, rearrange the actin cytoskeleton to caus

242 lin and branch nucleation by Arp2/3 (but not G-actin recycling).

243 ated kinase and PKC prevented the decline in G-actin; reduced cofilin and HSP27 phosphoprotein conten

244 elated transcription factor (MRTF) family of G-actin-regulated cofactors.

245 beige adipocyte formation via control of the G-actin-regulated transcriptional coactivator myocardin-

246 inally, in inflammatory fluids, DBP binds to G-actin released from damaged cells, and this complex ma

247 In contrast, raising G-actin resulted in mitochondrial fragmentation and decr

248 periments revealed only one binding site for G-actin, results clearly indicate that more than one mol

249 A comparison of F-actin with G-actin reveals the conformational changes during filame

250 es from MRTF-A, and de novo formation of the G-actin-RPEL complex is impaired by a transferable facto

251 G-actin's role as a stabilizer of the PPP1R15-containing

252 ddition of VT to pyrene-labeled mutant yeast G-actin (S265C) produced a fluorescence excimer band, wh

253 The G-actin-sensing mechanism of MAL/MRTF-A resides in its N

254 tal data of Helfer et al. on the capping and G-actin sequestering activity of twinfilin.

255 Thymosin beta4 (Tbeta4), a G-actin-sequestering peptide, improves neurological outc

256 molecular insight into how the known F- and G-actin sites on cofilin interact with the filament, and

257 G-actin stimulates Ca(2+)-ATPase activity of the enzyme

258 These RPEL(MAL):G-actin structures explain the sequence conservation def

259 , the mechanism responsible for transport of G-actin substrate to the cell front is largely unknown;

260 ngly, 98% of parasite actin is maintained as G-actin, suggesting that filaments are rapidly assembled

261 sly that locking the hydrophobic loop to the G-actin surface by a disulfide bridge prevents filament

262 Profilin-dependent dissociation of G-actin-Tbeta4 complexes simultaneously liberates actin

263 ward the tip, even the concentration bump of G actin that they create before they jam is enough to sp

264 ic spines contain a locally enriched pool of G-actin that can be regulated by synaptic activity.

265 tive gel composed of structural filaments (e.g., actin) that are acted upon by motor proteins (e.g.,

266 nd mechanical properties of monomeric actin (G-actin), the trimer nucleus, and actin filaments (F-act

267 For hybrid G-actins, the muscle-like and yeastlike parts of the mol

268 teractions with polar groups on solvents and G-actin; the average absorption energy of the correspond

269 ud6 binds to both the tail of the formin and G-actin, thereby recruiting monomeric actin to the formi

270 ouse CAP1 interacts with ADF/cofilin and ADP-G-actin through its N-terminal alpha-helical and C-termi

271 ted transcriptional coactivators, which bind G-actin through their N-terminal RPEL domains.

272 restricting the free diffusion of cytosolic G-actin throughout the bundle and, in particular, its pe

273 is crucial for the conversion of monomeric (G)-actin to filamentous (F)-actin.

274 The regulation of binding of G-actin to cytoplasmic domains of cell surface receptors

275 nced cortical actin, as well as a shift from G-actin to F-actin.

276 VT causes pyrene-labeled G-actin to polymerize in low ionic strength buffer (G-bu

277 forward-directed fluid flow that transports G-actin to the leading edge.

278 a-actin altered the ratio of globular actin (G-actin) to filamentous actin in MEFs, with correspondin

279 Addition of actin monomer (G-actin) to growing actin filaments (F-actin) at the lea

280 Thus, Myo1c-facilitated G-actin transport might be a critical node for control o

281 or myosin contraction-driven motility; 2), a G-actin transport-limited motility model; 3), a simple m

282 tions of the local and global regimes of the G-actin transport.

283 re distributed throughout the lamellipod, F-/G-actin turnover is local, and diffusion plays little ro

284 d that cysteine 345 in subdomain 1 of mutant G-actin was cross-linked to native cysteine 62 on cofili

285 of the association of MIM with cortactin and G-actin was evaluated in NIH3T3 cells expressing several

286 arly indicate that more than one molecule of G-actin was needed for a regulatory effect on the pump.

287 In contrast, no binding of G-actin was observed in palmitoyl-oleoyl phosphatidylcho

288 yptic cofilin binding site in subdomain 2 in G-actin, we used transglutaminase-mediated cross-linking

289 more WASP homology 2 (WH2) domains that bind G-actin, whereas the CA extension binds the Arp2/3 compl

290 el of nuclear MRTF-A is regulated by nuclear G-actin, which binds to MRTF-A and promotes its nuclear

291 s at the filopodial tip require transport of G-actin, which enter the filopodial tube from the filopo

292 lays a more open nucleotide binding cleft on G-actin, which is typical of profilin:actin structures,

293 as restored by crude cell lysate or purified G-actin, which joined PPP1R15-PP1 to form a stable terna

294 Full-length MIM binds to G-actin with a similar affinity as N-WASP-VCA, a constit

295 e actin polymerization, although it bound to G-actin with high affinity.

296 we characterize the interaction of purified G-actin with isolated PMCA and examine the effect of G-a

297 Recombinant AtADF4 bound to monomeric actin (G-actin) with a marked preference for the ADP-loaded for

298 Oxidation of actin monomer (G-actin) with copper o-phenanthroline resulted in a rapi

299 leading to a rapid exchange of WASP, WIP and G-actin within the PLS, which, in turn, actively invades

300 s that maintain the pool of monomeric actin (G-actin) within cells of higher eukaryotes.