ライフサイエンスコーパス: cofilin

1 ced by genetic reduction of cofilin (APP/PS1;cofilin(+/-)).

2 nd MLC20 , but induced de-phosphorylation of cofilin.

3 contribute to the severing deficiency of S3D cofilin.

4 with activation of the actin severing factor cofilin.

5 -mediated phosphorylation of FAK (p-FAK) and cofilin.

6 odulation by the regulatory severing protein cofilin.

7 filament severing by the regulatory protein cofilin.

8 n positively regulates nuclear actin through Cofilin.

9 ty of the filamentous actin severing protein cofilin.

10 Loss of Fascin results in decreased nuclear Cofilin.

11 mutant filaments are more readily severed by cofilin.

12 e--> Dopamine Receptor--> Scribble--> Rac--> Cofilin.

13 than WT and more susceptible to severing by cofilin.

14 erlap with the binding regions of myosin and cofilin.

15 CR) by activating the actin-severing protein cofilin.

16 uggested overlapping functions for ADF and n-cofilin.

17 complex and prevent filament disassembly by cofilin.

18 their biochemical activities with or without cofilin.

19 hatase (SSH) to dephosphorylate and activate Cofilin.

20 4-3-3-dependent regulation of phosphorylated cofilin.

21 and phosphorylate the actin binding protein cofilin.

22 ctive, phosphorylated, actin-binding protein cofilin.

23 ng activity at boundaries compared to single cofilin.

24 active (S3A) but not inactive (S3E) form of cofilin.

25 imited to subunits directly contacting bound cofilin.

26 n assembly/disassembly dynamics, such as ADF/Cofilins.

27 mutants that lack the actin-severing protein cofilin 1 (CFL1).

28 2-fold), cyclophilin A (PPIA; 0.9-fold), and cofilin-1 (CFL1, 1.3-fold).

29 to the AC group of proteins, which includes cofilin-1 and destrin.

30 Knockdown of either ADF or cofilin-1 by RNA interference increased the paracellular

31 Here we determine the LIMK1:cofilin-1 co-crystal structure.

32 Loss of either ADF or cofilin-1 did not affect the steady-state morphology of

33 findings demonstrate novel roles for ADF and cofilin-1 in regulating the remodeling and permeability

34 We examined the roles of ADF and cofilin-1 in regulating the structure and functions of A

35 ronal morphology and dysregulation of LIMK-1/cofilin-1 pathway could affect the cognitive outcome aft

36 LIMK-1/cofilin-1 signaling pathway is known to be involved in t

37 he neural gene expression pattern of LIMK-1, cofilin-1, and beta-actin in all the experimental groups

38 protein levels of LIMK-1, cofilin-1, phospho-cofilin-1, and beta-actin in the whole brain lysates as

39 ed alpha-enolase, 14-3-3 protein zeta/delta, cofilin-1, and heat shock cognate 71 kDa protein as nove

40 of alpha-enolase, 14-3-3 protein zeta/delta, cofilin-1, and heat shock cognate 71 kDa protein into a

41 ance of actin dynamics through regulation of cofilin-1, and in executing learning and memory function

42 three focal proteins: vimentin, stathmin and cofilin-1, belonging to or involved in cytoskeletal orga

43 Additionally, cofilin-1, but not ADF, depletion increased epithelial p

44 ed with diminished protein levels of LIMK-1, cofilin-1, phospho-cofilin-1, and beta-actin in the whol

45 had abnormally high levels of phosphorylated cofilin-1.

46 one of the major actin-regulating proteins, cofilin-1.

47 ing (MAS) NMR of the muscle isoform of human cofilin 2 (CFL2) bound to F-actin.

48 In humans, cofilin-2 (CFL2) mutations have been associated with con

49 Cofilin-2 is an actin-binding protein that is predominan

50 Pharmacological stimulation of cofilin-2 phosphorylation and genetic overexpression of

51 n skeletal muscles and negligible amounts of cofilin-2 protein.

52 gates in humans and the first report to link cofilin-2 to cardiomyopathy.

53 Cofilin-2 was predominantly phosphorylated, rendering it

54 man CFL2 mutation, p.A35T, that first linked cofilin-2 with the human disease, we created a knock-in

55 egates in human myocardium were enriched for cofilin-2, an actin-depolymerizing protein known to part

56 here it activates the actin-severing protein cofilin [6, 7].

57 tudies have shown the critical importance of cofilin, a filamentous actin-severing protein, in actin

58 t the loss of Limk1, a negative regulator of cofilin, accelerates the rate of spinal commissural axon

59 ASP and no binding to the verprolin homology/cofilin/acidic (VCA) region.

60 her beta3-integrin signaling through FAK and cofilin (actin depolymerization factor) is necessary to

61 By coupling the stress-sensitive cofilin-actin interaction with the light-responsive Cry2

62 ellular stress-gated protein switch based on cofilin-actin rod formation, occurring in stressed neuro

63 neural fibrils, reactive oxygen species, and cofilin-actin rods, present numerous challenges in the d

64 Cofilin/actin-depolymerizing factor (ADF) proteins are c

65 with Hsp90, Coronin 1B, and SSH to regulate Cofilin activation and Arp2/3 complex localization at th

66 omechanistically, amyloid-beta insult caused cofilin activation and F-actin remodeling and decreased

67 We have previously shown that cofilin activation plays a pivotal role in Abeta-induced

68 a42 oligomers to beta1-integrin triggers the cofilin activation, and in turn, cofilin promotes the in

69 wnregulation of antioxidant gene expression, cofilin activation, and remodeling of the actin cytoskel

70 he necessity of an intact cAMP-PDE4-PKA-LIMK-cofilin activation-signaling pathway for sleep deprivati

71 These differences in ADF/Cofilin activities and mechanisms may be used in cells t

72 Our data show that Rac1 and cofilin activity are key to determining the rate of acqu

73 chronophin (CIN) spatiotemporally regulates cofilin activity at the cell edge to generate persistent

74 tive F-actin assembly results from increased cofilin activity in Pdk1-deficient MKs.

75 Furthermore, we find that the regulation of cofilin activity is an acute response to nerve injury in

76 The elevated cofilin activity is caused by cAMP-degrading phosphodies

77 and cell protrusions and that H2O2 inhibits cofilin activity through oxidation of cysteines 139 (C13

78 F-actin ring is formed through regulation of Cofilin activity to block cytokinesis progress after con

79 , although the signaling pathways regulating cofilin activity to control cell direction have been est

80 of-principle experiments show that elevating cofilin activity, through the loss of Limk1, results in

81 Members of the cofilin/ADF family of proteins sever actin filaments, in

82 lamin A/C for nuclear aberrations induced by Cofilin/ADF loss.

83 siRNA mediated silencing of Cofilin/ADF provokes striking nuclear defects including

84 Consequently, cofilin/ADF Ser3 phosphorylation is tightly controlled a

85 Here we identify that Cofilin/ADF-family F-actin remodeling proteins are essen

86 endocytic actin patch ABPs fimbrin Fim1 and cofilin Adf1 enhances their activities, and prevents tro

87 ) isoforms influences disassembly induced by Cofilin alone, or by the collaborative effects of Cofili

88 vity, forming clusters of contiguously bound cofilin along the filament lattice.

89 es actin activity through phosphorylation of cofilin, an actin-depolymerizing factor.

90 09 tandem site controls its association with cofilin and actin and is important for CAP1 to regulate

91 Site-directed mutagenesis of both cofilin and actin revealed residues critical for sustain

92 Cofilin and actin-interacting protein 1 (AIP1; also know

93 Impeding Sh1 growth by RNAi to cofilin and Arp2/3 perturbed the DTC-Sh1 interface, redu

94 Actin-severing proteins such as cofilin and contractile myosin motor proteins fragment t

95 his was associated with changes to calponin, cofilin and HSP20 phosphorylated/total protein levels.

96 and this defect is due to hyperactivation of cofilin and inefficient actin polymerization.

97 contrast LAR activation inactivated PKCzeta, cofilin and LKB1.

98 These signaling changes inhibit cofilin and matrix metalloproteinases reducing in vitro

99 cts actin filaments from depolymerization by cofilin and myosin and indicate a mechanism by which SEP

100 ts reveal a synergistic relationship between cofilin and myosin II that is spatiotemporally regulated

101 d that C9ORF72 was present in a complex with cofilin and other actin binding proteins.

102 characterized by an increased activity of n-cofilin and profilin 1, leading to a thickened cortical

103 Cofilin and Profilin, which regulate the nuclear import

104 orylation of the synaptic plasticity markers cofilin and synapsin in the adult mouse hippocampus.

105 eads to the downregulation of phosphorylated cofilin and the resultant activated cofilin-induced modu

106 scent of eukaryotic actin modulators such as cofilin and thymosin beta4 and arcadin-2 is a depolymeri

107 min, profilin, tropomyosin, capping protein, cofilin, and AIP1) are sufficient to reconstitute the fo

108 endomitosis regulators LIM domain kinase 1, cofilin, and Aurora A/B/C.

109 g, which activates a host dependency factor, cofilin, and its kinase, the LIM domain kinase (LIMK).

110 n hippocampal cAMP-CREB-BDNF, cAMP-PKA-LIMK1-cofilin, and RhoA-ROCK2 pathways.

111 o with a higher cooperativity than wild-type cofilin, and severs actin weakly across a broad range of

112 of MK2 (MAPK-activated protein kinase 2) and cofilin, and signaling through CaMKII.

113 dampen platelet activation responses in a n-cofilin- and profilin 1-dependent manner, thereby indire

114 ial organization of F-actin as controlled by Cofilin, Anillin, and Septin.

115 ignificantly reduced by genetic reduction of cofilin (APP/PS1;cofilin(+/-)).

116 filaments that are partially decorated with cofilin are mechanically heterogeneous (i.e., nonuniform

117 Recent studies have found that LIMK/cofilin are targeted by viruses such as HIV-1 for propel

118 Two ADF/cofilin family members, ADF and n-cofilin, are highly abundant in the brain, where they ar

119 This pinpoints ADF/cofilin as a key regulator of axon growth competence, ir

120 racterized lysine 112 of the actin regulator cofilin as a novel neddylation event.

121 ing of actin filaments is mainly achieved by cofilin, assisted by Aip1/Wdr1 and coronins.

122 rments, whereas site-specific neddylation of cofilin at K112 regulates neurite outgrowth, suggesting

123 Phosphorylation of vertebrate cofilin at Ser-3 regulates both actin binding and severi

124 1B, known to regulate the Arp2/3 complex and Cofilin at the leading edge.

125 reveal the structural origins of cooperative cofilin binding and actin filament severing.

126 d CLIK-1 share common functions that inhibit cofilin binding and allow tropomyosin binding to actin f

127 while tension surprisingly has no effect on cofilin binding and weakly enhances severing.

128 in filaments and promotes highly cooperative cofilin binding to actin to create long stretches of pol

129 ses the fluorescence 20-fold, how myosin and cofilin binding to filaments reduces the fluorescence, a

130 ls and in vitro The S3D substitution weakens cofilin binding to filaments, and it is presumed that su

131 TPM decoration restricted Cofilin binding to pointed ends, while not interfering w

132 istorts the DNase binding loop, which allows cofilin binding, and a network of interactions among S14

133 F/cofilin-induced torque does not hinder ADF/cofilin binding, but dramatically enhances severing.

134 s on F-actin coupled to nucleotide-dependent cofilin binding, is sufficient to generate a form of act

135 r twist, experience a mechanical torque upon cofilin binding.

136 ng, Ser-3 modification favors formation of a cofilin-binding mode that is unable to sufficiently alte

137 Cofilin binds actin filaments with positive cooperativit

138 ansporters and the actin-controlling protein cofilin but does not depend on major Ca(2+)-dependent ca

139 LC20 , MYPT-1 and the actin-severing protein cofilin, but not of RhoA, ROCK2 or c-Src.

140 MSec also similarly inactivates cofilin, but potentiates TNT formation independent of th

141 Local depletion of ADF/Cofilin by binding to actin is significant, leading to w

142 Conversely, reduction of endogenous cofilin by knockdown or genetic deficiency inhibits mito

143 le tropomyosin offers little protection from cofilin cleavage, unlike its effect on WT actin.

144 Cofilin clusters disrupt both protofilaments, consistent

145 Filaments with small cofilin clusters were predicted to fragment within the c

146 e structures, with the distribution of bound cofilin clusters, suggest that maximum binding cooperati

147 Mammals express three different ADF/Cofilins (Cof1, Cof2, and ADF), and genetic studies sugg

148 An isolated, bound cofilin compromises longitudinal filament contacts of 1

149 f key parameters, such as actin density, ADF/Cofilin concentration and network width on the network l

150 length as a function of width, actin and ADF/Cofilin concentrations.

151 e data indicate that beta3-integrin, FAK and cofilin constitute a signaling pathway downstream of MMP

152 Actin depolymerizing factor (ADF)/cofilin controls actin turnover to sustain axon regenera

153 disassembly of heterogeneous networks by ADF/Cofilin controls steering during motility.

154 These findings taken together indicate that cofilin coopts and requires the nuclear and mitochondria

155 in alone, or by the collaborative effects of Cofilin, Coronin, and AIP1 (CCA).

156 early model proposed that the combination of cofilin, coronin, and Aip1 disassembled filaments in bur

157 -GTP content, SrcFK auto-phosphorylation and cofilin de-phosphorylation.

158 referentially at boundaries between bare and cofilin-decorated (cofilactin) segments and is biased at

159 labeled AIP1 during the severing process of cofilin-decorated actin filaments.

160 d preferentially at the boundary between the cofilin-decorated and bare regions on actin filaments.

161 Filaments with a single bare/cofilin-decorated boundary localize energy and force adj

162 molecules interact with the pointed ends of Cofilin-decorated filaments for several seconds at a tim

163 Boundaries between bare and cofilin-decorated segments are brittle and fragment at s

164 lastic energy at boundaries between bare and cofilin-decorated segments because of their nonuniform e

165 breaking network nodes, proportional to ADF/Cofilin density and inversely proportional to the square

166 nguished and yoked saline, and the p-FAK and cofilin depended on beta3-integrin signaling.

167 hyperactivation accompanied by catastrophic cofilin-dependent decreases in actin filament density, s

168 5-HT simultaneously induces cofilin-dependent decreases in actin network density and

169 increase the rate of growth cone advance via cofilin-dependent increases in retrograde actin network

170 he leading edge in a PI3-kinase-, Rac1-, and cofilin-dependent manner after EGF stimulation to activa

171 Unlike profilin, cofilin, Dia2, and N-WASP, they do not require high "sti

172 binding proteins (ABPs), including profilin, cofilin, Dia2, N-WASP, ezrin, and moesin, but the underl

173 Profilin and cofilin display transient, low-affinity interactions wit

174 ccupancy, whereas filament twisting enhances cofilin dissociation without compromising filament integ

175 ic nerve injury, the level of phosphorylated cofilin dramatically increases at the lesion site, in a

176 rmined by electron cryomicroscopy reveal how cofilin enhances the bending and twisting compliance of

177 imally influenced the effects of TGF-beta on cofilin expression and phosphorylation.

178 ents by either cytochalasin-D or conditional Cofilin expression resulted in decreased synaptic OXT le

179 ins of the actin depolymerizing factor (ADF)/cofilin family are the central regulators of actin filam

180 Two ADF/cofilin family members, ADF and n-cofilin, are highly ab

181 many actin-binding proteins, among which the cofilin family plays unique and essential role in accele

182 ross-linked filament networks are severed by cofilin far more efficiently than nonconnected filaments

183 tin filaments, most likely by competing with cofilin for binding to the side of actin filaments, redu

184 dicated that AMPK leads to the liberation of cofilin from 14-3-3 protein.

185 zymes releases the PI(4,5)P2-binding protein cofilin from its inactive membrane-associated state into

186 Suppression of cofilin function prevents spine loss, deficits in hippoc

187 First, the high cooperativity of S3D cofilin generates fewer boundaries between bare and deco

188 In addition, Fascin and Cofilin genetically interact, as double heterozygotes ex

189 All three ADF/Cofilins had similar affinities for G-actin and F-actin.

190 of 1 protofilament, consistent with a single cofilin having filament-severing activity.

191 Expression of oxidation-resistant cofilin impairs cell spreading, adhesion, and directiona

192 ken together indicate a significant role for cofilin in Abeta accumulation via dual and opposing endo

193 However, a role for cofilin in APP processing and Abeta metabolism has not b

194 Dual role of cofilin in APP trafficking and amyloid-beta clearance.

195 In this study, we found that knockdown of cofilin in Chinese hamster ovary 7WD10 cells and primary

196 vity of phosphorylation of FAK (p-FAK) and p-cofilin in dendrites of reinstated animals compared with

197 e, we monitor and quantify the action of ADF/cofilin in different mechanical situations by using sing

198 he expression, distribution, and activity of cofilin in human tissue and generated a cardiac-specific

199 is important for regulation of the roles of cofilin in severing and stabilizing actin filaments.

200 However, the expression of p-cofilin in the DKO mice was significantly decreased.

201 g either activated Rac1 or dominant-negative cofilin in the mushroom bodies (MBs) abolishes experienc

202 vation of the actin depolymerization protein cofilin in the olfactory system and in the hippocampus.

203 ownstream target, the actin-severing protein cofilin, in alcohol consumption preference.

204 We find that the Arp2/3 complex and cofilin, in turn, regulate the binding of tropomyosin to

205 ject to negative regulation by PLD1 thorough cofilin inactivation and inhibition of cofilin/p53 compl

206 We also modeled cofilin inactivity in vitro by using pharmacological and

207 cular dynamics simulations, we show that S3D cofilin indeed binds filaments with lower affinity, but

208 d an actin-cofilactin boundary indicate that cofilin-induced actin conformational changes are local a

209 orylated cofilin and the resultant activated cofilin-induced modulation of actin dynamics.

210 We find that this ADF/cofilin-induced torque does not hinder ADF/cofilin bindi

211 imental observations, indicates that the ADF/cofilin-induced torque increases the severing rate const

212 to polarized cell motility through localized cofilin inhibition and that there are additional protein

213 Cofilin is an actin filament severing protein necessary

214 Their cofilin is mostly unphosphorylated and associated with F

215 A key function of ADF/cofilin is to sever actin filaments.

216 Finally, activated cofilin is unable to induce apoptosis in cells genetical

217 leading edge dynamics by controlling active cofilin levels to promote MTLn3 cell protrusion.

218 a/beta, chemerin and its receptor ChemR23, p-cofilin, LIMK2 and PTEN and inhibiting BRAF and NLRX1 in

219 versely, dominant-negative Rac1 or activated cofilin MB expression lead to faster acquisition of alco

220 been previously reported that Aip1 regulates cofilin-mediated actin depolymerization, which is requir

221 Coronin and Aip1 promote cofilin-mediated actin filament disassembly, but the mec

222 d of neurons; it also specifically regulates cofilin-mediated actin remodeling that underlies the mat

223 lament stability, actin branch formation, or cofilin-mediated actin severing or how cortactin influen

224 s fiber maturation additionally requires ADF/cofilin-mediated disassembly of non-contractile stress f

225 hich is controlled by myosin contraction and cofilin-mediated disassembly.

226 Cofilin-mediated severing accelerates the turnover and s

227 ind that Mical oxidation of actin allows for cofilin-mediated severing even in the presence of inorga

228 We demonstrate that cofilin-mediated severing is a single-timescale mode of

229 It has been shown in vitro that cofilin-mediated severing of Arp2/3 actin networks resul

230 density gradients were controlled by higher cofilin-mediated turnover of F-actin in the front.

231 Thus, in conjunction with cofilin, Mical oxidation of actin promotes F-actin disas

232 Primary microglia isolated from cofilin(+/-) mice demonstrate significantly enhanced sta

233 ever, the reduction of Abeta load in APP/PS1;cofilin(+/-) mice is paradoxically associated with signi

234 ent OPCs by inhibiting non-canonical Hh-RhoA-Cofilin/MLC2 signalling.

235 nanometer resolution maps of isolated, bound cofilin molecules and an actin-cofilactin boundary indic

236 ldrich syndrome protein-interacting protein, cofilin, Munc13-4, and nonmuscle myosin IIA (NMIIA).

237 nin 1B together with a constitutively active Cofilin mutant.

238 tations of both capping protein subunits and cofilin mutations with severing defects, but no genetic

239 osphorylation) "undocks" and repositions the cofilin N terminus away from the filament axis, which co

240 regulates neurite outgrowth, suggesting that cofilin neddylation contributes to the regulation of neu

241 In the presence of ADF/Cofilin, networks reached equilibrium and became treadmi

242 it is presumed that subsequent reduction in cofilin occupancy inhibits filament severing, but this h

243 in filament severing with minimal effects on cofilin occupancy, whereas filament twisting enhances co

244 mum binding cooperativity is achieved when 2 cofilins occupy adjacent sites.

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

246 Second, S3D cofilin only weakly alters filament bending and twisting

247 This cofilin-p53 pro-apoptotic pathway is subject to negative

248 rough cofilin inactivation and inhibition of cofilin/p53 complex formation.

249 We show that the cofilin phosphatase chronophin (CIN) spatiotemporally re

250 or by increased Rac1/PAK- and LIMK-dependent cofilin phosphorylation and actin polymerization in dend

251 16), effects of G-1 on CA1 spine density and cofilin phosphorylation depended on JNK phosphorylation

252 NK kinases (>400-fold), potent inhibition of cofilin phosphorylation in A7r5, PC-3, and CEM-SS T cell

253 at position 3 (S3D) is widely used to mimic cofilin phosphorylation in cells and in vitro The S3D su

254 on by in vitro kinase assays, examination of cofilin phosphorylation in mammalian cells, and function

255 and found that cue-induced signaling through cofilin phosphorylation occurred only in D1-expressing n

256 ent with our previous findings, E(2)-induced cofilin phosphorylation was not dependent on GPER activa

257 BDNF-mediated stimulation of RhoA activity, cofilin phosphorylation, and actin polymerization were c

258 se signaling changes and downstream aberrant cofilin phosphorylation.

259 ng, and facilitated RhoA/ROCK/LIMK1-mediated cofilin phosphorylation.

260 RASSF1A blocked tumor growth by stimulating cofilin/PP2A-mediated dephosphorylation of the guanine n

261 Cofilin preferentially interacts with older filaments by

262 controlled by the actin regulatory proteins cofilin, profilin, and formin, which sever, recycle, and

263 Cofilin promotes phosphate dissociation and severs filam

264 riggers the cofilin activation, and in turn, cofilin promotes the internalization of surface beta1-in

265 ent manner after EGF stimulation to activate cofilin, promotes actin free barbed end formation, accel

266 of the actin-depolymerizing factor (ADF) and cofilin protein family play key roles in actin dynamics

267 evering by actin-depolymerizing factor (ADF)/Cofilin proteins.

268 ssion of active (S3A) but not inactive (S3E) cofilin reduces sAPP levels by enhancing APP endocytosis

269 The severing protein, cofilin, renders filaments more compliant in bending and

270 brain lysates as well as formation of actin-cofilin rods in the brain sections of symptomatic mice w

271 ochemical mechanism is critical to boost ADF/cofilin's ability to sever highly connected filament net

272 rom the filament axis, which compromises S3D cofilin's ability to weaken longitudinal filament subuni

273 k1-T423/p-P38-T180/p-MK2-T334/p-Limk1-S323/p-Cofilin-S3 molecular pathway.

274 timulated NOM by triggering a reduction of p-Cofilin-S3, a growth cone collapse marker, through decre

275 In this study, we show that activated cofilin (S3A) preferentially forms a complex with p53 an

276 e that high concentrations of yeast or human cofilin sever actin filaments, most likely by competing

277 Arg greatly potentiates cofilin severing of actin filaments, and cortactin atten

278 5 function prevents changes in cAMP-PKA-LIMK-cofilin signaling and cognitive deficits associated with

279 Additionally, beta1 integrin-cofilin signaling was triggered by the exposure and corr

280 s and memory consolidation depend on JNK and cofilin signaling, supporting a critical role for actin

281 xis and adhesion downstream of the ROCK-LIMK-cofilin signalling axis.

282 lation of the actin polymerization regulator cofilin, suggesting that activation of GPER may increase

283 well as its substrates LIM domain kinase and cofilin, supporting the hypothesis that the defective F-

284 ow that Cyclase-associated protein (CAP) and Cofilin synergize to processively depolymerize actin fil

285 , reducing the occupancy of the filaments by cofilin to a range favorable for severing.

286 Our results suggest that reduced binding of cofilin to actin filaments may be the underlying cause o

287 ay that terminates in the activation of Rac1/Cofilin to effect changes in the actin cytoskeleton and

288 ation of the F-actin depolymerization factor cofilin to induce TNT formation.

289 ulates F-actin remodeling by phosphorylating cofilin to inhibit actin severing and depolymerization.

290 hanges to the cortical actin-binding protein cofilin to stimulate the depolymerizing arm of the cycle

291 gue of the vertebrate actin-severing protein Cofilin, to regulate F-actin levels and apical cell memb

292 In the absence of coronin 1B or cofilin, Tpm1.8/9 protein levels are reduced while, conv

293 Phosphorylation of cofilin was enhanced in C9ORF72-depleted motor neurons,

294 medium spiny neurons (MSNs), but increased p-cofilin was observed only in D1-MSNs.

295 trophils and a new twist in the interplay of cofilin, Wdr1, and coronin in regulating F-actin dynamic

296 NCAM fragment interacts via PSA with PC4 and cofilin, which are involved in RNA polymerase II-depende

297 izing factors, and elevated levels of active cofilin, which mediates actin depolymerization.

298 gment is mediated by positive cofactor 4 and cofilin, which we identified as novel PSA-binding protei

299 An individual, bound phosphomimetic (S3D) cofilin with weak severing activity adopts a unique bind

300 sically and genetically with Rac1, Pak3, and Cofilin within MBn, nucleating a forgetting signalosome