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 oses via actomyosin contraction coupled with actin depolymerization.

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

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

6 recognized as a key regulator that promotes actin depolymerization.

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

8 6-propionyl-2-(N,N-dimethylamino)naphthalene actin depolymerization.

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

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

11 tubule-depolymerizing reagents but not after actin depolymerization.

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

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

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

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

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

17 mechanisms involving RhoA glucosylation and actin depolymerization.

18 ing tyrosine phosphorylation of paxillin and 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 clusters whose disassembly is maintained by actin depolymerization.

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

24 Leptin signaling also leads to F-actin depolymerization.

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

26 which mediates smooth muscle relaxation via actin depolymerization.

27 that these domains function independently in actin depolymerization.

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

29 chemistry progressively altered our views of actin depolymerization.

30 on of myosin light chain phosphorylation and actin depolymerization.

31 uld affect many biochemical reactions beyond actin depolymerization.

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

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

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

35 des stabilizing the filaments and preventing actin depolymerization.

36 re maintained and became highly mobile after actin depolymerization.

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

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

39 However, actin depolymerization also inhibits bud growth, suggest

40 Actin depolymerization also was achieved in pollen by tr

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

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

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

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

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

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

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

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

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

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

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

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

53 Calcium acts by promoting actin depolymerization and localizing actin polymerizati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 Actin depolymerization blocks the increase in spEPSC amp

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

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

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

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

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

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

77 Furthermore actin depolymerization by itself induces altered lipid r

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

79 Actin depolymerization can trigger microtubule depolymer

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

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

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

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

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

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

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

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

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

89 Actin depolymerization did cause Swe1p-dependent arrest

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

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

92 Actin depolymerization disrupts TJ structure and barrier

93 Both the actin depolymerization drug latrunculin B and the actin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 The actin depolymerization has been suggested to promote vir

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 Fast actin depolymerization is necessary for cells to rapidly

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 Declustering induced via either actin depolymerization or alkaline phosphatase treatment

152 Actin depolymerization or ATP depletion caused a two- to

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

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

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

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

157 Interestingly, F-actin depolymerization partially restored receptor mobil

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

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

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

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

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

163 The actin depolymerization promoted by YpkA was only seen in

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

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

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

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

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

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

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

171 Actin depolymerization resulted in Kv2.1 exocytosis at c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 Actin depolymerization was induced with latrunculin A (L

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

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

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

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

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

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

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

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

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

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

197 AMPK induces actin depolymerization, which reduces vascular tone and

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

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

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