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1 interest as they bind to G-actin and enhance actin polymerization.
2 bited neutrophil migration and intracellular actin polymerization.
3 ion, impairing N-WASP-driven Arp2/3-mediated actin polymerization.
4 domain but not the TOCA1 HR1 domain inhibits actin polymerization.
5 te smoke extract via oxidative disruption of actin polymerization.
6 supports memory by directly driving synaptic actin polymerization.
7 ulinum toxin substrate 1 GTPase activity and actin polymerization.
8 ation of T cell receptor-driven (TCR-driven) actin polymerization.
9 fectors such as N-WASP that induce localized actin polymerization.
10 bles microtubular transport, exocytosis, and actin polymerization.
11 enance of total actin levels and preserves F-actin polymerization.
12 contractility of smooth muscle by regulating actin polymerization.
13 5)P2 and PI(3)P in a curved vesicle triggers actin polymerization.
14 -regulation of a large number of genes after actin polymerization.
15 ntegrin activation by fibronectin to nuclear actin polymerization.
16 trosylation of cytosolic actin that enhances actin polymerization.
17 th micromolar affinities and weakly nucleate actin polymerization.
18 actin assembly proteins, formins, to sustain actin polymerization.
19 me, across multiple contexts, and depends on actin polymerization.
20 P-mediated molecular processes necessary for actin polymerization.
21 es the actin cortex rearward to facilitate f-actin polymerization.
22 and prolonged the effects of BDNF and TEA on actin polymerization.
23 suppresses UNC-73 function and, indirectly, actin polymerization.
24 ile myosin-II activity and not to elevated F-actin polymerization.
25 o hyperactivation of cofilin and inefficient actin polymerization.
26 e to ACh, and also inhibited contraction and actin polymerization.
27 , proliferation, autophagy, translation, and actin polymerization.
28 rocess akin to blebbing and is not driven by actin polymerization.
29 a permissive open conformation, speeding up actin polymerization.
30 Uptake was dependent on dynamin and actin polymerization.
31 elated protein 2/3 (Arp2/3) complex-mediated actin polymerization.
32 ange depends on strong synaptic activity and actin polymerization.
33 ependent, Abl/Src tyrosine kinase-mediated F-actin polymerization.
34 negative regulator of RhoGTPase activity and actin polymerization.
35 d that it regulates contraction by mediating actin polymerization.
36 bles microtubular transport, exocytosis, and actin polymerization.
37 Rho-kinase signaling pathways and stimulated actin polymerization.
38 ctic signal transduction network, as well as actin polymerization.
39 -readout, likely downstream of PCP-regulated actin polymerization.
43 ssociated inverted formin-2 (INF2), a potent actin polymerization activator (mutations of which are a
45 These effects are due to Cyfip1's role in actin polymerization and are reversed by expression of a
46 ion as SRF coactivators, serve as sensors of actin polymerization and are sequestered in the cytoplas
47 rate the crucial role of Skap2 in regulating actin polymerization and binding of talin-1 and kindlin-
48 on effector protein that plays roles in both actin polymerization and caspase-3 activation in intesti
51 this network is required to link stimuli to actin polymerization and chemotactic motility and we dis
54 ldrich syndrome protein (N-WASP) activation, actin polymerization and contraction in response to ACh.
56 The primary drivers of yeast endocytosis are actin polymerization and curvature-generating proteins,
57 rotein-based network of 14 genes involved in actin polymerization and dendritic spine formation (nomi
59 at fragmentation of murine ovaries increases actin polymerization and disrupts Hippo signaling, leadi
61 ed protein kinase 2 (MK2) pathway to promote actin polymerization and endothelial cell migration.
62 ling through c-Src and Cdc42, which modulate actin polymerization and filopodia formation via the Arp
63 signal-regulated kinase phosphorylation and actin polymerization and for L-Phe-induced Ca(2+)i mobil
64 method is then used to treat the dynamics of actin polymerization and force generation during endocyt
66 tructures has been correlated with increased actin polymerization and global organization of the acti
67 PAK1 signaling to N-WASP-cortactin-mediated actin polymerization and GLUT4 vesicle translocation.
69 e protrusion, we find that Mena11a decreases actin polymerization and growth factor-stimulated membra
70 to IL-20 that manifested as modification of actin polymerization and inhibition of a broad range of
72 genes.Trio is a RhoGEF protein that promotes actin polymerization and is implicated in the regulation
73 actin-related protein 2/3 (Arp2/3)-dependent actin polymerization and is involved in regulating the t
74 of constitutively active mutant ADF reduces actin polymerization and junctional protein disassembly,
78 letal organization by studying the effect of actin polymerization and nuclear rigidity on the diffusi
79 lonRI in processes that depend on stimulated actin polymerization and outward trafficking of REs.
80 e mediated by cytoskeletal changes involving actin polymerization and p38 mitogen-activated protein k
81 a phosphorylated state, thereby decreasing F-actin polymerization and preventing cell migration in a
82 n-binding protein that promotes formin-based actin polymerization and regulates numerous cellular fun
83 ytochalasin D (CytoD) and PP2, inhibitors of actin polymerization and Src activity, respectively.
85 y mDia1 and Fmnl3 as major factors enhancing actin polymerization and stabilizing E-cadherin at epith
86 moting actin depolymerization and localizing actin polymerization and the actin nucleation promotion
87 ctivation of ROCK/MLC signalling, persistent actin polymerization and the disassembly of junctional p
88 imary PIP3-stimulated Rac activator, whereas actin polymerization and the GTPase-activating protein A
91 ith the important role of Pfn1 in regulating actin polymerization and various fundamental actin-based
93 , phosphatidylinositol-3-OH kinase, PAK1 and actin polymerization, and activated upon Cdc42 inhibitio
94 the smooth muscle cell cortex, via cortical actin polymerization, and by downstream smooth muscle ef
96 ng, possibly through its ability to regulate actin polymerization, and inhibiting its activity could
98 cium channels, protein kinase C, Rho-kinase, actin polymerization, and myocardin-related transcriptio
99 my1 proteins, which bind formins and inhibit actin polymerization, and myosin motors, which deliver S
101 ndent mb-KitL/c-kit clustering, anchorage, F-actin polymerization, and Tyr567-dependent cluster phosp
104 clear magnetic resonance and the pointed-end actin polymerization assay, we find that leiomodin-2, a
106 the contribution of myosin contraction, and actin polymerization at bundles' terminals when the prod
107 ds on F-actin, but the mechanisms regulating actin polymerization at cell-cell junctions remain poorl
109 ntiated NB4 cell migration and intracellular actin polymerization at concentrations seen during acute
110 wn is the mechanism triggering INF2-mediated actin polymerization at ER-mitochondria intersections.
111 s myosin II-derived force inhibits vectorial actin polymerization at focal adhesions through AMPK-med
113 tor SopE, we recapitulated Rho GTPase-driven actin polymerization at model phospholipid membrane bila
114 sidues, in particular tyrosine 421, promotes actin polymerization at newly-forming invadopodia, promo
115 tochastic simulations of force generation by actin polymerization at obstacles coated with actin "nuc
117 rotein complex, which has been implicated in actin polymerization at synapses, a process thought to b
119 tion or blockade on T cells caused defective actin polymerization at the contact site with APC, alter
120 Cortical retrograde flow resulting from actin polymerization at the edges is shown to be modulat
121 abarti et al. demonstrate that INF2 mediates actin polymerization at the endoplasmic reticulum (ER),
122 is eliminated there is negligible effect on actin polymerization at the immunological synapse, leadi
123 formin (FMN)-type actin nucleators initiate actin polymerization at vesicular membranes necessary fo
126 ata suggest that the Arp2/3 complex-mediated actin polymerization brings two opposing membranes into
127 s also exhibit a normal initial magnitude of actin polymerization but fail to polarize actin assembly
128 lators that target the FH2 domain to inhibit actin polymerization, but little is known about how thes
129 Mechanoactivation of the AT1 R stimulates actin polymerization by a protein kinase C-dependent mec
130 tin filament length regulator that repressed actin polymerization by binding to monomeric actin.
132 otide exchange factor (RhoGEF) Trio promotes actin polymerization by directly activating the small GT
133 timulated phosphoprotein (VASP) can catalyze actin polymerization by elongating actin filaments.
138 confirm this hypothesis for mDia1 dependent actin polymerization by stretching a single-actin filame
139 force for constriction is thought to involve actin polymerization by the ER-anchored isoform of the f
142 supports a general mechanism where localized actin polymerization can coordinate activation of the co
145 t activates the small GTPase, cdc42, and the actin polymerization catalyst, neuronal Wiskott-Aldrich
146 the absence of CD37 in neutrophils impaired actin polymerization, cell spreading and polarization, d
149 ntrast, jasplakinolide, a drug that enhances actin polymerization, consolidates the cytoskeleton netw
150 rodents and that the loss of mTORC2-mediated actin polymerization contributes to age-associated memor
151 n-related transcription factor (MRTF), a Rho/actin polymerization-controlled coactivator of serum res
153 The regulation of EAAT2 expression involves actin polymerization-dependent activation of the transcr
157 -Aldrich syndrome protein (N-WASP)-activated actin polymerization drives extension of invadopodia and
158 prisingly, a possibility that unextinguished actin polymerization drives neurite outgrowth in the pre
159 beta-catenin with N-cadherin is regulated by actin polymerization during contractile activation.
162 on of increased coat rigidity and force from actin polymerization enables robust vesiculation even at
164 sphorylation attenuates MCP1-induced HASMC G-actin polymerization, F-actin stress fiber formation, an
165 sphorylation, cortactin-WAVE2 interaction, G-actin polymerization, F-actin stress fiber formation, an
166 ortactin interaction with WAVE2, affecting G-actin polymerization, F-actin stress fiber formation, an
167 s singled out the actin cytoskeleton and the actin polymerization factor, the Arp2/3 complex, as top
168 ssembly, previous studies suggest that other actin polymerization factors, such as formins, may parti
170 ynamics, but the mechanisms steering nascent actin polymerization for cell-cell adhesion initiation a
171 palmitoylation is essential for normal spine actin polymerization, for spine-specific structural plas
172 e found to be microtubule associated, making actin polymerization from microtubule-associated platfor
174 ated that N-WASP is required for localized F-actin polymerization, GLUT4 vesicle translocation, and g
175 icate that the cyto-D treatment blocking the actin polymerization has a dominant effect at the large
176 x and branched actin networks soften it, but actin polymerization has no effect on cortex stiffness.
178 uss here the propagation of forces caused by actin polymerization, highlighting simple configurations
179 onsistent with HSPB7's inhibitory effects on actin polymerization, HSPB7 KO mice had longer actin/thi
180 dynamin oligomerization and thus, increases actin polymerization, improved renal health in diverse m
186 depolymerizing factor (ADF) causes sustained actin polymerization in ECs, whereas EC-targeted overexp
188 t dynamin oligomerization and thus increased actin polymerization in injured podocytes, was sufficien
189 bl-related gene (Arg) activation, leading to actin polymerization in invadopodia, extracellular matri
190 risingly important role for CRMP-1, EVL, and actin polymerization in maintaining the structural integ
191 sits that attractive guidance cues stimulate actin polymerization in neuronal growth cones whereas re
192 This change triggers otherwise-forbidden actin polymerization in primary cilia, which excises cil
193 in light chain phosphorylation at Ser-19 and actin polymerization in response to contractile activati
194 tion of the cytoskeleton involving increased actin polymerization in response to Rho-associated kinas
196 1a can dampen membrane protrusion and reduce actin polymerization in the absence of other Mena isofor
197 therapeutic effect is reversed by inhibiting actin polymerization in the CD36(+/+) macrophages, suppo
198 ex, and therefore suggest a role for nuclear actin polymerization in the context of cellular adhesion
199 ures that can mitigate the effect of Pfn1 on actin polymerization in vitro As a further proof-of-conc
201 f MKL1 expression in MZMs led to defective F-actin polymerization, inability to clear ACs, and, event
202 Our results show that myosin II activity and actin polymerization increase cortex tension and intrace
203 ollicular fluid constituent known to promote actin polymerization, increased the conversion of globul
205 a Trio-Rho/Rac signaling circuitry promoting actin polymerization, independently of phospholipase Cbe
207 les E-cadherin to the actin cytoskeleton, or actin polymerization inhibitors similarly attenuated DR4
212 se results indicate that formin-based linear actin polymerization is critical for the formation and m
217 hat Drp1 binds actin filaments directly, and actin polymerization is necessary for mitochondrial Drp1
220 ons remain as to how force generated through actin polymerization is transmitted to the plasma membra
222 ngle actin filament elongation, we show that actin polymerization kinetics at both filament ends are
223 d raise concerns about the interpretation of actin polymerization kinetics based solely on protein de
229 oting invadopodium maturation and consequent actin polymerization, matrix degradation, and invasive m
230 ovide new insights into how Arp2/3-dependent actin polymerization modulates both Kv3.3 activity and i
231 as an effector of WASP-mediated control over actin polymerization, mutations in protein components of
235 nd actin depolymerization, whereas increased actin polymerization offers protective effects and incre
245 its signaling pathway, leading to defective actin polymerization, platelet activation, and shape cha
246 that the final steps of extravasation, where actin polymerization plays an important role, are impair
248 e ovaries with muM Jasplakinolide (JASP), an actin polymerization-promoting cyclic peptide, or sphing
249 olve actin polymerization, we tested whether actin polymerization-promoting drugs could promote YAP t
251 ners of CRB3 in the testis were the branched actin polymerization protein Arp3, and the barbed end-ca
252 of Arp3 (actin-related protein 3, a branched actin polymerization protein) and palladin (an actin bun
253 that both proteins are involved in explosive actin polymerization, pseudopod formation, and cell migr
254 hanistically, this phenomenon is mediated by actin polymerization, Rac1 activation, and alphaIIbbeta3
255 s in the model: substrate adhesion strength, actin polymerization rate, myosin contractility, and the
258 protrusion waves are due to fluctuations in actin polymerization rates and that overexpression of VA
259 in as bait to recruit and phosphorylate host actin polymerization-regulating proteins, including the
261 gers local Rac-GTP hydrolysis, thus reducing actin polymerization required for filopodia formation.
262 Further, we find that this force-promoted actin polymerization requires torsionally unconstrained
263 Cytochalasin-D, to inhibit beta-integrin or actin polymerization, respectively, significantly reduce
265 nitiation, proximally localized Mwh inhibits actin polymerization resulting in polarized activation o
268 n assays, live-cell imaging of motility, and actin polymerization studies to confirm a role for CD13
269 an actin anti-capping protein that promotes actin polymerization, switches highly adherent keratocyt
271 courses and the effects of interventions on actin polymerization: the surprising increase in the pea
272 he downstream Rho GTPase effectors mediating actin polymerization through Arp2/3 nucleation, Wiskott-
274 extracellular matrix interaction to nuclear actin polymerization through the LINC complex, and there
275 of endocytic sites is essential for allowing actin polymerization to drive membrane invagination.
278 ction is important to transduce the force of actin polymerization to the membrane to drive successful
279 lly inhibit and thereby polarize Rac1-driven actin polymerization to the protrusions of migratory fib
280 IG-2, which function redundantly to polarize actin polymerization upstream of the WAVE complex and WA
281 at CD73-generated adenosine induces cortical actin polymerization via adenosine A1 receptor (A1R) ind
282 ical role at the SF-FA junction by promoting actin polymerization via free barbed end generation and
287 t not myosin light chain phosphorylation and actin polymerization, was reduced by the expression of t
288 opography can unidirectionally bias internal actin polymerization waves and that cells move with the
289 use these damaging procedures likely involve actin polymerization, we tested whether actin polymeriza
290 RhoA activity, cofilin phosphorylation, and actin polymerization were completely suppressed by prote
292 sed by TGF-beta/Smads, GPCR/Rho signals, and actin polymerization, whereas GPCR/cAMP signals and acti
293 Mena interacts with GRASP65 to promote local actin polymerization, which facilitates Golgi ribbon lin
294 in complex and unravel that FURIN promotes F-actin polymerization, which has previously been shown to
295 f the cytoskeletal protein HS1, along with F-actin polymerization, which resulted in rapid receptor i
296 mplex (WRC) to drive Arp2/3 complex-mediated actin polymerization, which underpins diverse cellular p
297 es microtubule organization as inhibition of actin polymerization with a low dose of latrunculin A di
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