ライフサイエンスコーパス: cofilin

1 than WT and more susceptible to severing by cofilin.

2 erlap with the binding regions of myosin and cofilin.

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

4 uggested overlapping functions for ADF and n-cofilin.

5 complex and prevent filament disassembly by cofilin.

6 their biochemical activities with or without cofilin.

7 hatase (SSH) to dephosphorylate and activate Cofilin.

8 4-3-3-dependent regulation of phosphorylated cofilin.

9 cap the barbed ends of filaments severed by cofilin.

10 es the extent of F-actin depolymerization by cofilin.

11 INF2 is a more potent severing protein than cofilin.

12 large part by pharmacological activation of cofilin.

13 actin toward the actin-depolymerizing factor cofilin.

14 and its downstream F-actin regulatory factor cofilin.

15 th that of the well-studied severing protein cofilin.

16 ls that are enriched with Arp2/3 complex and cofilin.

17 ents even in the presence of high amounts of cofilin.

18 orylation of the actin-depolymerizing factor cofilin.

19 ctin severing and depolymerizing activity of cofilin.

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

21 which leads to activation of PI3K/Akt and n-cofilin.

22 activity of the actin depolymerizing protein Cofilin.

23 dent on localized F-actin disassembly by ADF/cofilin.

24 contribute to the severing deficiency of S3D cofilin.

25 with activation of the actin severing factor cofilin.

26 odulation by the regulatory severing protein cofilin.

27 filament severing by the regulatory protein cofilin.

28 n positively regulates nuclear actin through Cofilin.

29 ty of the filamentous actin severing protein cofilin.

30 Loss of Fascin results in decreased nuclear Cofilin.

31 mutant filaments are more readily severed by cofilin.

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

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

34 an "actin nucleotide-state sensor" among ADF/cofilins.

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

36 on of MRTF-A import occurs via activation of cofilin 1 and inactivation of vasodilator-stimulated pho

37 can fully compensate for low levels of smn, cofilin 1, profilin 2 and alpha-actinin 1 did not affect

38 The actin filament severing protein cofilin-1 (CFL-1) is required for actin and P-type ATPas

39 2-fold), cyclophilin A (PPIA; 0.9-fold), and cofilin-1 (CFL1, 1.3-fold).

40 ve also defined in the actin-binding protein cofilin-1 a link between PP2A, actin cytoskeleton, and n

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

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

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

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

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

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

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

48 Ezrin-dependent actin remodeling involved cofilin-1 that is essential for the turnover and reorgan

49 Phosphorylated, inactive cofilin-1 was up-regulated in diabetic glomeruli, sugges

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

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

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

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

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

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

56 Cofilin-1-severing/depolymerization activity is negative

57 had abnormally high levels of phosphorylated cofilin-1.

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

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

60 In contrast to other isoforms, cofilin-2 efficiently binds and disassembles both ADP- a

61 The results suggest that cofilin-2 evolved specific biochemical and cellular prop

62 Cardiac-specific haploinsufficiency of cofilin-2 in mice recapitulated the human disease's morp

63 Our findings also offer a rationale for why cofilin-2 mutations in humans lead to myopathies.

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

65 demonstrate that the muscle-specific isoform cofilin-2 promotes actin filament disassembly in sarcome

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

67 Cofilin-2 was predominantly phosphorylated, rendering it

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

69 We mapped surface-exposed cofilin-2-specific residues required for ATP-actin bindi

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

71 Cofilin, a critical player of actin dynamics, is spatial

72 n of the actin cytoskeleton specifically via Cofilin, a key regulator of F-actin assembly.

73 The essential regulatory protein cofilin accelerates network remodeling by severing actin

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

75 that, besides driving the rapid severing of cofilin-actin filaments, Aip1 also augments the monomer

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

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

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

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

80 Dysfunction in PAK leads to cofilin activation, drebrin displacement from its actin-

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

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

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

84 mice) to characterize the importance of ADF/cofilin activity for synapse physiology and mouse behavi

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

86 in motor neurons demonstrates that increased Cofilin activity promotes rapid bouton formation in resp

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

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

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

90 on CXCL12/CXCR4 signalling and increased ADF/Cofilin activity.

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

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

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

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

95 that actin disassembly is controlled not by cofilin alone, but by a more complex set of factors work

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

97 , and inactivation of the Rho target protein cofilin, an actin-depolymerizing factor.

98 east Srv2/CAP, mouse CAP1 interacts with ADF/cofilin and ADP-G-actin through its N-terminal alpha-hel

99 rks have remained elusive; however, Coronin, Cofilin and AIP1 have been implicated in this process.

100 hosphorylation of actin-disassembling enzyme cofilin and glutamate receptor GluR1, resulting in abnor

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

102 KC prevented the decline in G-actin; reduced cofilin and HSP27 phosphoprotein content, respectively;

103 d G-actin content and elevated the levels of cofilin and HSP27 phosphorylation.

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

105 lting in dephosphorylation and activation of cofilin and leading to enhanced cell migration.

106 contrast LAR activation inactivated PKCzeta, cofilin and LKB1.

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

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

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

110 Cofilin and Profilin, which regulate the nuclear import

111 echanism by which the combined activities of cofilin and Srv2/CAP lead to enhanced filament severing

112 OCK1- and LIMK1-regulated phosphorylation of cofilin and subsequent local disruption of dynamic actin

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

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

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

116 ta1 activation, involving the LIMK effectors cofilin and TPPP/p25, for assembly of the actin- and tub

117 n of the actin regulatory factors cortactin, cofilin, and Arp2/3 complexes, suggesting that disassemb

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

119 phosphorylated LC(20), calponin, caldesmon, cofilin, and HSP27, as well as G-actin content, were det

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

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

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

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

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

125 s, pulling by type V myosin, and severing by cofilin are simulated as growth, cross-linking, pulling,

126 the elevation of McTNs and the activation of cofilin are specific results arising from PTEN loss.

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

128 Actin depolymerizing factor (ADF)/cofilins are essential regulators of actin turnover in e

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

130 tis elegans, we have identified UNC-60A (ADF/cofilin) as an essential regulator of invadopodia.

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

132 d modulate actin dynamics by phosphorylating cofilin at serine-3.

133 1B, known to regulate the Arp2/3 complex and Cofilin at the leading edge.

134 At high concentrations ADF/cofilins bind stably to F-actin longitudinally between t

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

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

137 INF2, like cofilin, binds stoichiometrically to filament sides and

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

139 howed that RhoE activates podosome component cofilin by inhibiting its Rock-mediated phosphorylation.

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

141 Cofilin (CFL) is an F-actin-severing protein required fo

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

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

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

145 -Thr508/505-LIMK1/2, as well as phospho-Ser3-cofilin, compared with wild-type normal MSCs.

146 However, the cofilin concentration in thymocytes is too high to allow

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

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

149 ull cells exhibited evidence of dysregulated cofilin de/phosphorylation pathways.

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

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

152 lin rescues the viability of a S. cerevisiae cofilin deletion mutant only when the stiffness cation s

153 Our results indicate that Aip1 is a cofilin-dependent actin depolymerization factor and not

154 e in cytosolic pH at invadopodia and blocked cofilin-dependent actin polymerization, leading to impai

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

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

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

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

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

160 ADF/cofilins drive cytoskeletal dynamics by promoting the di

161 Although cofilin effects on actin filament assembly dynamics have

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

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

164 ins of the actin depolymerizing factor (ADF)/cofilin family are essential for actin dynamics, which i

165 ins of the actin-depolymerizing factor (ADF)/cofilin family have been shown to be crucial for the mot

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

167 by a mechanism similar to that of other ADF/cofilin family members, displaying a preference for ADP-

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

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

170 ious studies demonstrated the relevance of n-cofilin for postsynaptic plasticity, associative learnin

171 -binding site may be universally used by ADF/cofilins for actin filament severing.

172 In the stabilization phase, cofilin formed a stable complex with F-actin, was persis

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

174 ts C-terminal-half catalyzes dissociation of cofilin from ADP-actin monomers and stimulates nucleotid

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

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

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

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

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

180 Cofilin has a crucial role in the nucleation of these F-

181 the cytosol via the VCA (verprolin-homology, cofilin-homology, and acidic) domain and support RNA pol

182 In contrast to cofilin, however, INF2 binds ADP and ADP-Pi filaments eq

183 e blocking of the decoration site with human cofilin (HsCOF1) using cytochalasin D increases its seve

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

185 2 that also inhibited the direct biomarker p-cofilin in cells and inhibited the invasion of MDA MB-23

186 lament severing is the essential function of cofilin in cells.

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

188 ression of constitutively active or inactive Cofilin in motor neurons demonstrates that increased Cof

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

190 d engages actin dynamics via Rho-GTPases and cofilin in this process.

191 PfADF1 is unique among ADF/cofilins in being able to sever F-actin but do so withou

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

193 Low densities of ADF/cofilins, in contrast, result in the optimal severing of

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

195 ase signaling pathway in DCs, which controls cofilin inactivation and myosin II activation and, there

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

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

198 ore, phosphorylation modulators of HSP27 and cofilin induced significant changes in arterial diameter

199 ensively studied, the molecular mechanism of cofilin-induced filament severing is not understood.

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

201 erizer system, the actin-remodelling protein cofilin induces dramatic changes in the F-actin network

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

203 , the overexpression of Limk, which inhibits Cofilin, inhibits bouton budding.

204 at the use of a partially impaired mutant of cofilin is critical for maintaining low background activ

205 e that actin filament severing by vertebrate cofilin is driven by the linked dissociation of a single

206 Cofilin is necessary for actin disassembly in cells, and

207 role of the actin filament severing protein cofilin is now firmly established; however, the contribu

208 Cofilin is spatiotemporally regulated; at the plasma mem

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

210 Mammals express several ADF/cofilin isoforms, but their specific biochemical activit

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

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

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

214 Aip1 inverts the rules of cofilin-mediated actin disassembly such that increasing

215 prevailing model of actin filament turnover--cofilin-mediated actin filament severing--can account fo

216 Our model supports a direct role for cofilin-mediated actin polymerization in stimulated cell

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

218 th the suppression of ROCK and activation of cofilin-mediated actin reorganization, plays a key role

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

220 ted inhibition of actin-spectrin binding and cofilin-mediated depolymerization of actin filaments, pl

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

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

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

224 over: its hexameric N-terminal-half enhances cofilin-mediated severing of filaments, while its C-term

225 r, are capable of severing, while measurable cofilin-mediated severing requires more extensive bindin

226 Moreover, N-CAP1 enhances yeast cofilin-mediated severing, and conversely, yeast N-Srv2

227 and conversely, yeast N-Srv2 enhances human cofilin-mediated severing, highlighting the mechanistic

228 ts, altering F-actin structure and enhancing cofilin-mediated severing.

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

230 ore, a regulatory loop consisting of SRF and cofilin might take part in reactivating actin dynamics i

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

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

233 ing, actin patches assembled slowly in these cofilin mutant cells.

234 Finally, a cofilin mutant that mimics phosphorylated Ser-3 can part

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

236 directed recruitment of the reduced activity cofilin mutants to the cytoskeleton is sufficient to ind

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

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

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

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

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

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

243 Vertebrate cofilin only weakly severs Saccharomyces cerevisiae acti

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

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

246 turation by acting upstream of the ROCK-LIMK-Cofilin pathway through the control of RhoC GTPase activ

247 We conclude that the RhoE-Rock-cofilin pathway, by promoting podosome dynamics and patt

248 actin filament and the malaria parasite ADF/cofilin, PfADF1 from Plasmodium falciparum.

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 of RhoA or Rac1 blocked effects of folate on cofilin phosphorylation and cellular migration and invas

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 ion of LIMK1 activity and down-regulation of cofilin phosphorylation in response to aluminum fluoride

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

257 enchymal-to-epithelial transition, decreased COFILIN phosphorylation, and disrupted Actin filament st

258 beta treatment increased LIMK-2 activity and cofilin phosphorylation, decreasing filopodia formation.

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

260 e inhibitor of LIMK1 activity that prevented cofilin phosphorylation.

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

262 Cofilin preferentially interacts with older filaments by

263 Cofilin promotes phosphate dissociation and severs filam

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

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

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

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

268 Moreover, vertebrate cofilin rescues the viability of a S. cerevisiae cofilin

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

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

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

272 chanisms in cells to switch from a regime of cofilin-saturation and stabilization to one that favors

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

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

275 5 function prevents changes in cAMP-PKA-LIMK-cofilin signaling and cognitive deficits associated with

276 elevance of the LRAP25-MRCK complex in LIMK1-cofilin signaling and the importance of LRAP adaptors as

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

278 nd electron microscopic studies on ADF and n-cofilin single mutants and double mutants (named ACC mic

279 tin ratios, whereas higher concentrations of cofilin suppress severing.

280 ation of Rac results in dephosphorylation of cofilin that can promote actin polymerization and format

281 Inhibiting cofilin, the primary downstream target of PAK and a majo

282 ADP-actin monomers, while in the presence of cofilin this activity additionally requires the WH2 doma

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

284 n disassembly such that increasing ratios of cofilin to actin now result in filament destabilization

285 it severs filaments most efficiently at low cofilin to actin ratios, whereas higher concentrations o

286 rates with actin-depolymerizing factor (ADF)/cofilin to disassemble actin filaments in vitro and in v

287 karyotic organisms, where it cooperates with cofilin to disassemble actin filaments, but neither its

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

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

290 is work is the first to directly link an ADF/cofilin to the cytoskeletal rearrangements elicited dire

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

292 the muscle-specific, actin-severing protein cofilin (unc-60) suppress the axon phenotype, suggesting

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

294 Furthermore, McTNs were suppressed and cofilin was inactivated by restoration of PTEN in the PT

295 oskeleton was rapidly remodeled while active cofilin was massively transported to the spine.

296 n of the downstream Pak1 effectors LIMK1 and cofilin was reduced in growth cones from NCAM-deficient

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

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

299 Furthermore, cofilin, whose activation is associated with actin skele

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