ライフサイエンスコーパス: actin depolymerization

1 han the disassembly rate (corresponding to F-actin depolymerization).

2 orrelate with changes in cell morphology and actin depolymerization.

3 ux, to inhibition of PI3K activity, and to F-actin depolymerization.

4 Both these effects and RVD were reduced by actin depolymerization.

5 recognized as a key regulator that promotes actin depolymerization.

6 IM-kinase/cofilin phosphorylation leading to actin depolymerization.

7 6-propionyl-2-(N,N-dimethylamino)naphthalene actin depolymerization.

8 ytotoxicity (measured by 51Cr release) and F-actin depolymerization.

9 filament ends, and enhance profilin-mediated actin depolymerization.

10 tubule-depolymerizing reagents but not after actin depolymerization.

11 large-budded cells to arrest in response to actin depolymerization.

12 ivation, and both processes are sensitive to actin depolymerization.

13 cement insensitive to both I(h) blockers and actin depolymerization.

14 vesicle recycling are largely resistant to F-actin depolymerization.

15 leavage and loss of viability in response to actin depolymerization.

16 mechanisms involving RhoA glucosylation and actin depolymerization.

17 ing tyrosine phosphorylation of paxillin and actin depolymerization.

18 oses via actomyosin contraction coupled with actin depolymerization.

19 phin-glycoprotein complex had no effect on F-actin depolymerization.

20 twork may account for a part of the observed actin depolymerization.

21 in vascular endothelial monolayers through f-actin depolymerization.

22 s were disrupted, characterized by increased actin depolymerization.

23 effects on cholesterol lowering pathways or actin depolymerization.

24 lin-1 binding to F-actin and cofilin-induced actin depolymerization.

25 ted levels of active cofilin, which mediates actin depolymerization.

26 clusters whose disassembly is maintained by actin depolymerization.

27 nd to similar ER phenotype as observed after actin depolymerization.

28 Leptin signaling also leads to F-actin depolymerization.

29 before vs. 0.6 +/- 0.2 pN/mum after partial actin depolymerization.

30 which mediates smooth muscle relaxation via actin depolymerization.

31 that these domains function independently in actin depolymerization.

32 binding domain and delays dilution-induced F-actin depolymerization.

33 chemistry progressively altered our views of actin depolymerization.

34 on of myosin light chain phosphorylation and actin depolymerization.

35 uld affect many biochemical reactions beyond actin depolymerization.

36 ns, paxillin and talin, and an impairment in actin depolymerization.

37 h defect that is as severe as that caused by actin depolymerization.

38 errations, cell-wall defects, and defects in actin depolymerization.

39 des stabilizing the filaments and preventing actin depolymerization.

40 re maintained and became highly mobile after actin depolymerization.

41 alcium sensitivity of the mutant G1-G3 for F-actin depolymerization activity, although the F-actin-bi

42 ctin accumulations consistent with a lack of actin depolymerization activity.

43 However, actin depolymerization also inhibits bud growth, suggest

44 Actin depolymerization also was achieved in pollen by tr

45 Moreover, we find that actin depolymerization and AMPA receptor exocytosis are

46 leading to dendritic spine shrinkage through actin depolymerization and AMPAR depression through rece

47 ee-dimensional growth, latrunculin-A-induced actin depolymerization and apoptosis, and cell line tran

48 y which Clostridium difficile toxin A causes actin depolymerization and cell rounding involves toxin

49 ersed the effects of chronic ethanol on both actin depolymerization and dopamine release.

50 CeTM inhibited UNC-60B-induced actin depolymerization and enhancement of actin polymeri

51 , association of villin with PIP(2) inhibits actin depolymerization and enhances actin cross-linking

52 bition of the RhoA-signaling pathway induced actin depolymerization and facilitated exocytosis.

53 axons is commonly ascribed to signaling of F-actin depolymerization and growth cone collapse by molec

54 of Latrunculin B, a reagent known to induce actin depolymerization and impair bulk and ultrafast end

55 ession and leading to faster glucose-induced actin depolymerization and increased insulin release.

56 the flavin monooxygenase enzyme that induces actin depolymerization and indirectly promotes serum res

57 Consistent with its role in actin depolymerization and KRAS signaling, loss of MICAL

58 Thus, both actin depolymerization and ligand-induced integrin confo

59 Calcium acts by promoting actin depolymerization and localizing actin polymerizati

60 myelin dependence as well as independence of actin depolymerization and microtubule disruption lead u

61 triction via filament sliding driven by both actin depolymerization and myosin II motor activity.

62 ophin-glycoprotein complex and its effect on actin depolymerization and polymerization were examined.

63 ating domain of MARTX(Vc) would accelerate F-actin depolymerization and provide G-actin, alone or in

64 iated counterpart, display the anticipated F-actin depolymerization and severing activities.

65 odeling the cytoskeleton through filamentous actin depolymerization and severing.

66 previously established that SI stimulates F-actin depolymerization and that altering actin dynamics

67 es coincident PtdIns(3,4,5)P3 generation and actin depolymerization, and could be inhibited by mechan

68 ithin 24 hours, consisting of cell rounding, actin depolymerization, and decreased focal adhesions.

69 s, including phagosomal maturation, possible actin depolymerization, and homotypic phagosome fusion,

70 surface expression by leptin is dependent on actin depolymerization, and pharmacologically induced ac

71 , resulting in the inhibition of tip growth, actin depolymerization, and programmed cell death (PCD).

72 Cl(-), water, and Ca(2+) influx, and spine F-actin depolymerization are all necessary, but not indivi

73 Strikingly, actin depolymerization, as well as destabilization of in

74 Using F-actin co-sedimentation and actin depolymerization assays in vitro and fluorescence

75 se that fascin-2 crosslinks function to slow actin depolymerization at stereocilia tips to maintain s

76 Tropomyosin alone also inhibits the rate of actin depolymerization at the pointed end of filaments.

77 Our data imply a new mechanism: actin depolymerization-based force retracts the cell rea

78 However, inhibition of actin depolymerization blocked the expression of LTD, su

79 Actin depolymerization blocks the increase in spEPSC amp

80 Gnb5 knockout did not influence cortical actin depolymerization but affected protein kinase C act

81 athway downstream of G protein signaling and actin depolymerization but upstream of insulin granule r

82 naptic transmission is inhibited by block of actin depolymerization, but Ca(2)(+) signalling is unaff

83 at dystrophin-glycoprotein complex inhibited actin depolymerization by capping the ends of actin fila

84 r results suggest an allosteric mechanism of actin depolymerization by cofilin.

85 SEPT9 significantly reduces the extent of F-actin depolymerization by cofilin.

86 al RTX toxin, which causes cell rounding and actin depolymerization by covalently cross-linking actin

87 nd the binding of gelsolin to LTA inhibits F-actin depolymerization by gelsolin.

88 Furthermore actin depolymerization by itself induces altered lipid r

89 calcium-sensitive sites in villin, regulate actin depolymerization by villin.

90 Actin depolymerization can trigger microtubule depolymer

91 Finally, transient actin depolymerization caused many cells to abandon one

92 experimental observation that inhibition of actin depolymerization causes retrograde flow to slow ex

93 Thus, LatA-induced actin depolymerization causes TJ structural and function

94 However, unlike actin depolymerization, Cdk1 inhibition does not result

95 i; live-cell imaging additionally shows that actin depolymerization coincides with EGFP-OCRL-a accumu

96 We propose that during exocytosis, actin depolymerization commences near the secretory orga

97 always required, and there is evidence that actin depolymerization contributes to contraction.

98 main (ACD) cross-links G-actin, leading to F-actin depolymerization, cytoskeleton rearrangements, and

99 Depletion of either SNX27 or VPS35 or actin depolymerization decreased the rate of PTHR recycl

100 Actin depolymerization did cause Swe1p-dependent arrest

101 ed in a 25-mV hyperpolarizing shift, whereas actin depolymerization did not alter the activation midp

102 Drug-induced F-actin depolymerization disrupted both the apicobasal-lik

103 Actin depolymerization disrupts TJ structure and barrier

104 Both the actin depolymerization drug latrunculin B and the actin

105 hese observations suggest that OCRL promotes actin depolymerization during L. monocytogenes infection

106 lities of the actin cytoskeleton and altered actin depolymerization dynamics in response to latruncul

107 tor-stimulated phosphoprotein, and increased actin depolymerization [e.g., reduced LIM (Lin11/Isl-1/M

108 c1, notably, p21-activated kinase (Pak1) and actin depolymerization factor (ADF) promoted evoked secr

109 -interacting protein 1, which interacts with actin depolymerization factor (ADF) to enhance the rate

110 olecular dynamics, how the severing protein, actin depolymerization factor (ADF)/cofilin, modulates t

111 ts indicate that Aip1 is a cofilin-dependent actin depolymerization factor and not a barbed-end-cappi

112 Here we show that the actin depolymerization factor cofilin is essential for a

113 he phosphorylation and inactivation of the F-actin depolymerization factor cofilin to induce TNT form

114 he phosphorylation and inactivation of the F-actin depolymerization factor cofilin to induce TNT form

115 ilin is an actin-binding protein and a major actin depolymerization factor in the central nervous sys

116 -integrin signaling through FAK and cofilin (actin depolymerization factor) is necessary to promote s

117 Tsr), the Drosophila homolog of Cofilin/ADF (actin depolymerization factor), is a component of the cy

118 s the actin cytoskeleton by sequestering the actin depolymerization factor, cofilin, to reduce actin

119 actin polymerization by phosphorylating the actin depolymerization factor, cofilin.

120 ncluded a beta-expansin expressed in shoots, actin depolymerization factor, inositol-3-phosphate synt

121 n to require the deactivation of Cofilin, an actin depolymerization factor.

122 Glia maturation factor-gamma (GMFG), a novel actin depolymerization factor/cofilin superfamily protei

123 c and cell biology-based analyses, show that actin-depolymerization factor 4 (ADF4) is a physiologica

124 hological changes required regulation of the actin-depolymerization factor cofilin at a conserved LIM

125 sistent with this possibility, we found that actin depolymerization fails to induce a G2/M delay once

126 lux, tyrosine phosphorylation of MAPKs or in actin depolymerization following activation.

127 s its dependence on Ca(2+) or low pH for the actin depolymerization function, interestingly, G1-G2 an

128 confirmed that Glu-16 is critical for the F-actin depolymerization function.

129 The actin depolymerization has been suggested to promote vir

130 at stimulation of BCR induces a rapid global actin depolymerization in a BCR signal strength-dependen

131 (CPD) is essential for this toxin to induce actin depolymerization in a broad range of cell types.

132 n response, and genetically controlled MT or actin depolymerization in embryos leads to disruption of

133 A role for calcium-dependent actin depolymerization in LTD of NMDAR EPSCs was support

134 We show that leptin-stimulated F-actin depolymerization in mouse hypothalamic cells is in

135 truction microscopy (dSTORM), we show that F-actin depolymerization in spines leads to a breakdown of

136 food reward, is vulnerable to disruption by actin depolymerization in the basolateral amygdala compl

137 ed the contraction rate and also the rate of actin depolymerization in the ring.

138 tracellular trypsin activation and excessive actin depolymerization in vitro and the severity of panc

139 Espin cross-links slowed actin depolymerization in vitro less than twofold.

140 imulated actin polymerization, and inhibited actin depolymerization in vitro.

141 in-1, an actin-binding protein that promotes actin depolymerization, in linking RhoA/ROCK pathway to

142 biological activities, including filamentous actin depolymerization, inactivation of RhoA, and inhibi

143 ause similar transformations, and found that actin depolymerization induced multiple axons in unpolar

144 th the less pronounced softening effects for actin depolymerization induced via latrunculin A.

145 ent with latrunculin A, a drug that leads to actin depolymerization, induces dispersal of the Cdc42 m

146 olymerization of actin enhances and blocking actin depolymerization inhibits BCR signaling, leading t

147 to which overt structural changes occur with actin depolymerization is dependent on the severity and

148 Here, we report that actin depolymerization is essential for initiation of NG

149 Fast actin depolymerization is necessary for cells to rapidly

150 in A does not mimic MB, demonstrating that F-actin depolymerization is not responsible for unidirecti

151 However, D275R and A167R actin depolymerization is profound with cofilin.

152 olymerization, and pharmacologically induced actin depolymerization is sufficient to enhance Kv2.1 su

153 imental measurements support the notion that actin depolymerization is the predominant mechanism for

154 For example, actin depolymerization is thought to activate the morpho

155 collecting duct cells, filamentous actin (F-actin) depolymerization is a critical step in vasopressi

156 e mobility of the G1 domain, essential for F-actin depolymerization, is indirectly regulated by the g

157 eristic network architecture by showing that actin depolymerization leads to increased sheet fluctuat

158 ike complete actin depolymerization, partial actin depolymerization leads to the dispersal of Cdc42p

159 Potentially mediating this F-actin depolymerization, leptin, but not insulin, stimula

160 trate that SNRK knockdown promotes excessive actin depolymerization, measured by the increased ratio

161 t of neurotransmitter release is specific to actin depolymerization mediated by latrunculin A and is

162 ostsynaptic density (PSD), was unaffected by actin depolymerization, microtubule depolymerization, or

163 model of C. difficile adherence regulated by actin depolymerization, microtubule restructuring, subse

164 Therefore, the rate of actin depolymerization must be accelerated by one or mor

165 Blocking actin depolymerization, Na(+)/H(+) exchange, PI3K, and P

166 tdIns(4,5)P(2)), which triggered the partial actin depolymerization necessary for occupancy-elicited

167 re, F-actin becomes increasingly stable, but actin depolymerization no longer disrupts basic synaptic

168 the effect of latrunculin-B (Lat-B)-induced actin depolymerization on outflow physiology in live mic

169 Declustering induced via either actin depolymerization or alkaline phosphatase treatment

170 Actin depolymerization or ATP depletion caused a two- to

171 ndependent, and lasting disruption by direct actin depolymerization or by inhibiting the actin driver

172 very stable, because they are insensitive to actin depolymerization or inactivation of Rho kinase, wh

173 in different cell types, we demonstrate that actin depolymerization or stabilization and protein kina

174 is likely to contribute to stimulus-mediated actin depolymerization, our data suggest a role for addi

175 risingly, we now report that unlike complete actin depolymerization, partial actin depolymerization l

176 Interestingly, F-actin depolymerization partially restored receptor mobil

177 ecruitment of dynein to the actin cortex, as actin depolymerization phenocopies dynein depletion, and

178 intermediate for nucleotide exchange in the actin depolymerization/polymerization cycle.

179 g new HSP70 transgene/speckle association by actin depolymerization prevented significant heat shock-

180 usoidal endothelial cells, and blocking of F-actin depolymerization prevented the increase in matrix

181 olymerization, whereas GPCR/cAMP signals and actin depolymerization promote Ski protein stability.

182 The actin depolymerization promoted by YpkA was only seen in

183 quired for initiation of myelination whereas actin depolymerization promotes myelin wrapping.

184 icates, paradoxically, that a faster rate of actin depolymerization promotes net polymerization.

185 and inversal FRAP experiments show that the actin depolymerization promotes the dissociation of V1-V

186 sticity by controlling the activation of the actin depolymerization protein cofilin in the olfactory

187 n G-actin polymerization and a decrease in F-actin depolymerization rates in pyren-actin fluorescence

188 Actin depolymerization reagent latrunculin-B (Lat-B) abo

189 Both glucose stimulation and F-actin depolymerization recruit a fraction of nearly immo

190 se of the leading edge, which suggested that actin depolymerization regulated microcluster flow and t

191 stingly, the enhancement of Sox9 function by actin depolymerization requires both protein kinase A (P

192 Actin depolymerization resulted in Kv2.1 exocytosis at c

193 rget gene and that genotoxic stress triggers actin depolymerization, resulting in actin-stress-fiber

194 During the first week in culture, actin depolymerization results in a near complete loss o

195 fect of dystrophin-glycoprotein complex on F-actin depolymerization saturated at a dystrophin:actin m

196 in displacement from its actin-binding site, actin depolymerization/severing, and, ultimately, defect

197 teady-state measurements of gelsolin-induced actin depolymerization suggest that half-maximum depolym

198 os mimic those observed after drug-induced F-actin depolymerization, suggesting that the combined act

199 rization or genetically mediated decrease of actin depolymerization suppresses the nuf mutant F-actin

200 n and migration, which was associated with F-actin depolymerization, suppression of PDGF-induced Rac1

201 Following osmotic shock or actin depolymerization, Swe1p is stabilized, and previou

202 role for oxidoreduction in triggering local actin depolymerization to control HIV-1 budding, a mecha

203 cells might be able to tune the mechanism of actin depolymerization to meet physiological demands and

204 We previously demonstrated that actin depolymerization under force is governed by catch-

205 activation increased cofilin activity and F-actin depolymerization via an ERK-dependent mechanism.

206 reduced ability of lysine mutants to mediate actin depolymerization via filament disassembly although

207 Calcium-induced F-actin depolymerization was attenuated in the presence of

208 , demonstrating that the loss of GIP-induced actin depolymerization was indeed limiting insulin exocy

209 Actin depolymerization was induced with latrunculin A (L

210 ligand-induced binding site expression when actin depolymerization was inhibited by jasplakinolide,

211 ment cytoskeleton, we sought to determine if actin depolymerization was sufficient to induce apoptosi

212 ause growth cone collapse is associated with actin depolymerization, we considered whether small GTP-

213 cludin internalization and TER loss, but not actin depolymerization, were blocked at 14 degrees C, su

214 -transformed cells but actually led to rapid actin depolymerization when these cells were exposed to

215 the presence of Latrunculin A (which induces actin depolymerization), when added after granule polari

216 ath is increased by both sodium blockade and actin depolymerization, whereas increased actin polymeri

217 Exocytosis requires actin depolymerization which is actively counteracted un

218 anchor on the postsynaptic membrane involves actin depolymerization, which allows the released AMPARs

219 und that TNFalpha induces geometry-dependent actin depolymerization, which enhances IkappaB degradati

220 eported that Aip1 regulates cofilin-mediated actin depolymerization, which is required for normal neu

221 AMPK induces actin depolymerization, which reduces vascular tone and

222 a-accumbens latrunculin A or by accelerating actin depolymerization with a LIM-kinase inhibitor.

223 Finally, forced actin depolymerization with latrunculin B restored the e

224 In the absence of actin depolymerization, YY1 does not relocate to the nuc