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

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

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

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

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

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

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

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

13 ite complex additionally involving Cap1p and G-actin.

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

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

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

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

18 ysteines in the regions predicted to bind to 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 ll likely have increased levels of monomeric G-actin.

23 enriched PP1 cofactor that is controlled by G-actin.

24 PPP1R15-PP1 phosphatase identified monomeric G-actin.

25 s ability to polymerize as compared with ADP G-actin.

26 ly reduced the spontaneous polymerization of G-actin.

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

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

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

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

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

32 Profilins bind to globular (G-)actin and regulate actin filament formation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 ongation by binding to both monomeric actin (G-actin) and formin proteins.

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

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

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

56 ilin-1, colocalized in the terminal web with G-actin, and knockdown of this factor compromised brush

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

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

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

60 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

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

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

63 Potentiation or disruption of the G-actin/ArhGAP12 interaction, by treatment with the acti

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

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

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

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

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

69 uitous branched actin nucleator, to increase G-actin availability during brush border assembly.

70 Thus, brush border assembly is limited by G-actin availability, and profilin-1 directs unallocated

71 and we propose that this complex acetylates G-actin before it is incorporated into filaments.

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 this setting, ArhGAP12 mutants defective for G-actin binding exhibit more effective downregulation of

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

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

78 G-actin binding protein, profilin-1, colocalized in the

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

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

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

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 ha-SMA transcription and itself regulated by 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 RPEL proteins, which contain the G-actin-binding RPEL motif, coordinate cytoskeletal proc

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

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

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

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

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

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

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

101 Decreased monomeric G-actin but increased filamentous F-actin following CD44

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

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

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

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

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

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

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

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

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

111 We determine the structure of the ArhGAP12/G-actin complex, and show that G-actin contacts the RPEL

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

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

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

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

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

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

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

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

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

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

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

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

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

125 ArhGAP12 GAP activity, and this requires the G-actin contacts identified in the structure.

126 the ArhGAP12/G-actin complex, and show that G-actin contacts the RPEL motif and GAP domain sequences

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

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

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

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

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

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

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

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

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

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

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

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

139 tion barrier for pointed end polymerization, G-actin did not bind at an F-actin pointed end.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 re seen when the incoming subunit was in the G-actin form.

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

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

158 ft path for furrow ingression, and releasing G-actin from internal networks to build cortical network

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 G-actin inhibits ArhGAP12 GAP activity, and this require

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 ilament and has a conformation distinct from G-actin, meaning that incoming monomers would need to un

210 ntrol of sensory neuron activity by targeted G-actin modification.

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

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

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

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

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 rsecting signaling pathways, one mediated by G-actin/MRTF and the other via TGFbetaR/p38MAPK.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 s at the nuclear envelope, increased F-actin/G-actin ratios, and deregulation of mechanoresponsive my

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 identical to the ATP monomer, enhancing ATP G-actin's ability to polymerize as compared with ADP G-a

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

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

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

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

256 er growth were rescued by treatment with the G-actin sequestering drug, latrunculin A.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

275 mpounds affected the transition of monomeric G-actin to filamentous F-actin, and that several of thes

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 ddition, we identified profilin-1 (Pfn-1), a G-actin transporter, as a new partner for Abi1.

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

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

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

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

296 The interaction of G-actin with RPEL-family rhoGAPs thus provides a negativ

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.