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1 models proposing PMS as specialized cortical actin.
2 ization of YAP which led to an increase in F-actin.
3 on to their function as regulators of CP and actin.
4 on microscopy and by staining of filamentous actin.
5  changes thus led to a dis-organization of F-actin across Sertoli cell cytosol, causing truncation of
6 lated Myo2 were obtained that exhibited high actin-activated ATPase activity and in vitro actin filam
7              We demonstrate that the maximum actin-activated ATPase activity of M2beta-S1 is slowed m
8 nine and glutamic acid substitutions reduced actin-activated ATPase activity, slowed the in vitro sli
9  a twofold increase in the rate constant for actin-activated phosphate release, the biochemical step
10 he LIM domain kinase (LIMK), which regulates actin activity through phosphorylation of cofilin, an ac
11 in the initiation of BCR signaling caused by actin alteration is associated with a decreased humoral
12 ficient neutrophils are unable to polymerize actin and exhibit a block in both degranulation and DNA
13 maintaining the morphological structure of F-actin and in protein transport, loss of this function mi
14 behaviors require interaction of the dynamic actin and microtubule cytoskeleton.
15 tin monomers, suggesting competition between actin and microtubules for binding profilin.
16                                 Indeed, when actin and microtubules were present simultaneously, mela
17 activation of the PI3K, and recruitment of F-actin and of the actin-branching protein cortactin.
18                The structure of cofilin on F-actin and the details of the intermolecular interface re
19 efect in NADPH oxidase fail to induce either actin and tubulin polymerization or NET formation on act
20 ession and that GJA1-20k complexes with both actin and tubulin.
21 ed reduced myosin heavy chain, smooth muscle actin, and desmin, and increased markers of dedifferenti
22 imilar actin-binding proteins, interact with actin, and how this mechanism can be perturbed to cause
23 rdinates the polarized localization of MCAM, actin, and myosin IIB in a Wnt5a-induced manner.
24 cular bodies through mechanisms that involve actin- and microtubule-mediated motility, cytoskeleton-m
25 e mechanochemical behavior of stress fibers, actin arcs, and cortical actin-based structures.
26                  beta- and gamma-cytoplasmic actin are nearly indistinguishable in their amino acid s
27 oteins of these four chemotaxis pathways and actin are preferentially enriched at the cell front duri
28                                We found that actin, Arp2/3, vinculin and integrin-beta first accumula
29 sses and is based on contractility of random actin arrays.
30 ac/Rho family GTPases and by using monomeric actin as bait to recruit and phosphorylate host actin-re
31 ed ACF7, a crosslinker of microtubules and F-actin, as an essential player in this process.
32  and nucleated erythrocytes, due to impaired actin assembly and cytoskeleton stability.
33 te load is associated with an increase in F- actin assembly and NADPH oxidase activity.
34 ite-specific, lamellipodial versus cytosolic actin assembly and resulting consequences on protrusion.
35  of membrane-associated functions related to actin assembly and signaling.
36                       Despite protrusion and actin assembly defects, Arpc2(-/-) macrophages competent
37 an amended model of processive VASP-mediated actin assembly in clustered arrays.
38 w show that CRMP-1 is a major contributor to actin assembly in epithelial cells, where it works with
39 hate multikinase (IPMK) and promotes nuclear actin assembly that is required for ATR recruitment.
40 th WASP and SCAR/WAVE-activators of branched actin assembly-make actin-filled pseudopods.
41 serine/threonine kinase that associates with actin at the cellular leading edge of motile cells and s
42                        We demonstrate that F-actin automata implement OR, AND, XOR and AND-NOT gates
43  the cell periphery, where distinct types of actin-based membrane protrusions formed.
44 st position through an active, oriented, and actin-based migration dependent on Rac1, which contrasts
45 ndent phosphorylation on the activity of the actin-based Rab27a/melanophilin/myosin Va transport comp
46 r of stress fibers, actin arcs, and cortical actin-based structures.
47 b27a/melanophilin/myosin Va complex mediates actin-based transport in vivo.
48 on-dependent, substrate-parallel contractile actin belt at the apex that governs anaphase cell flatte
49 yosin motor domain that are triggered upon F-actin binding and contribute critically to the mechanoch
50 D) of beta-III-spectrin causes high-affinity actin binding and decreased thermal stability in vitro.
51 rmation in the presence of calcium, enabling actin binding and severing.
52 -iLID can be used to temporally recruit an F-actin binding domain to MT plus ends and cross-link the
53                     We show here that direct actin binding, via the inner centromere protein (INCENP)
54 eceptor ICAM-1 is negatively regulated by an actin-binding adaptor protein, i.e., CD2AP, to allow a b
55 r ataxia type 5 (SCA5) L253P mutation in the actin-binding domain (ABD) of beta-III-spectrin causes h
56                         Talin contains three actin-binding domains (ABDs).
57   Exon 16 of protein 4.1R encodes a spectrin/actin-binding peptide critical for erythrocyte membrane
58 [PI(4,5)P2], regulate the activities of many actin-binding proteins (ABPs), including profilin, cofil
59  the cytoskeleton in IECs via changes in the actin-binding proteins VIL1 and GSN.
60 ement in these processes is mediated by many actin-binding proteins, among which the cofilin family p
61  which beta-III-spectrin, and likely similar actin-binding proteins, interact with actin, and how thi
62 reas Tmods have alternating tropomyosin- and actin-binding sites (TMBS1, ABS1, TMBS2, ABS2), Lmods la
63 h, and comprise alternating tropomyosin- and actin-binding sites (TMBS1, ABS1, TMBS2, and ABS2).
64 s a 139-amino-acid protein containing five F-actin-binding sites and two G-actin-binding sites, and i
65 taining five F-actin-binding sites and two G-actin-binding sites, and interacts with wheat (Triticum
66 sion containing a proline-rich domain and an actin-binding Wiskott-Aldrich syndrome protein homology
67 , HGF induces both structural changes in the actin-bound junctional protein complex and physical forc
68  PI3K, and recruitment of F-actin and of the actin-branching protein cortactin.
69 ese in vivo findings indicated that abnormal actin bundles, not elongated thin filament length, were
70 tin polymerization protein) and palladin (an actin bundling protein).
71 ubule configuration, aligned with the apical actin cable and adherens-junctions within chick and mous
72 r trichome cells contained long longitudinal actin cables, the short Li1 fiber cells accumulated diso
73       Here we show that Mical-oxidized (Mox) actin can undergo extremely fast (84 subunits/s) disasse
74  that lamin A/C expressing cells can form an actin cap to resist nuclear deformation in response to p
75                   Finally, we show that both actin clearance and recovery correlated with synaptic ph
76 tes intracellular motility and spreading via actin comet tail formation.
77 lexes, including beta- and gamma-catenin and actin, components of adherens junctions (AJ).
78                     The remaining diffusible actin concentration is orders of magnitude higher than t
79 an 4-fold in the presence of OM, whereas the actin concentration required for half-maximal ATPase was
80 n linked to a change in the structure of the actin-containing thin filaments that allows the head or
81 Measuring the opening shape of the epidermal actin cortex after laser nano-ablation, we assess the sp
82   Our data underline the crucial role of the actin cortex in maintaining hindered diffusion modes of
83 tes for anchoring titin in the Z-disk is the actin cross-linker alpha-actinin.
84                                          The actin cross-linking protein Filamin has an important rol
85                                  The role of actin cross-linking proteins in cortical dynamics is sti
86  role for Plk4 in regulating Arp2/3-mediated actin cytoskeletal rearrangement.
87 iferation and modulates Rho-GTPase-dependent actin cytoskeletal signaling in fetal lungs.
88 dely studied for its role in controlling the actin cytoskeleton and plays a part in several potential
89 ires septin-dependent reorientation of the F-actin cytoskeleton at the base of the infection cell, wh
90 rmin protein essential for the regulation of actin cytoskeleton dynamics in diverse biological proces
91 ng evidence highlights the importance of the actin cytoskeleton in modulating inflammatory responses.
92            AIM1 strongly associates with the actin cytoskeleton in prostate epithelial cells in norma
93 e Ena/VASP family member EVL to assemble the actin cytoskeleton in the apical cortex and in protrudin
94 er depends on spatial control of dynamics of actin cytoskeleton in the foot processes.
95 lation-dependent excess stabilization of the actin cytoskeleton is a key phosphorylation-dependent me
96                                    A dynamic actin cytoskeleton is necessary for viral entry, intrace
97 pproaches to show that reorganisation of the actin cytoskeleton is required for dark-induced stomatal
98         Here we test the hypothesis that the actin cytoskeleton is the primary barrier to transcellul
99 eceptor tyrosine kinases that participate in actin cytoskeleton remodeling.
100 for Gag synthesis to non-PM membranes or the actin cytoskeleton severely reduced net virus particle p
101 taset showed enrichment in axon guidance and actin cytoskeleton signalling pathways as well as activa
102 I signal is mediated by rearrangement of the actin cytoskeleton, a process referred to as dynamic mas
103  appears to be an important modulator of the actin cytoskeleton, implicating maintenance of muscular
104 yndrome protein (WASp), which signals to the actin cytoskeleton, modulates autophagy and inflammasome
105 pendent of tyrosine kinase signaling and the actin cytoskeleton, suggesting selection for avid TCR mi
106 B share a common function in stabilizing the actin cytoskeleton, they physically interact in the cyto
107 ultiple signaling cascades that regulate the actin cytoskeleton, would compromise the structural stab
108 idency, as a crucial linker between kAE1 and actin cytoskeleton-associated proteins in polarized cell
109                                              Actin cytoskeleton-mediated FA growth and maturation thu
110 own as ermin) was initially identified as an actin cytoskeleton-related oligodendroglial protein in t
111 cular switches best known for regulating the actin cytoskeleton.
112 r reinforcement response that stabilizes the actin cytoskeleton.
113 e pathway through these macromolecules which actin-cytoskeleton-generated tensile force takes when ap
114 s tropomyosin in a blocked-state position on actin defined by a deeper energy minimum, consistent wit
115  2,4-D-induced inhibition of root growth and actin degradation compared with their respective parenta
116  These data reveal a liquid droplet phase of actin, demixed from the surrounding solution and dominat
117 ely targeting mitochondria, lysosomes, and F-actin demonstrate low toxicity and enable stimulated emi
118 echanism through which CTLs control cortical actin density.
119  of EGFP-labelled mitochondria occurs via an actin-dependent endocytic pathway which is consistent wi
120 erization and inhibition of a broad range of actin-dependent functions, including phagocytosis, granu
121                                 GBPs inhibit actin-dependent motility and cell-to-cell spread of bact
122 ee-dimensional growth, latrunculin-A-induced actin depolymerization and apoptosis, and cell line tran
123 ivity through phosphorylation of cofilin, an actin-depolymerizing factor.
124 fying polypeptides, which effectively induce actin disassembly in eukaryotic cells.
125 rotein gelsolin, and that gelsolin regulates actin disassembly in the connecting cilium, thus facilit
126 to combinatorially increase Mical-mediated F-actin disassembly, cellular remodeling, and repulsive ax
127 's M44 and M47 residues to induce cellular F-actin disassembly.
128 l to directly amplify Mical Redox-mediated F-actin disassembly.
129  initiator caspase dronc triggers cortical F-actin dismantling, enabling the glands to stretch as the
130 in-stimulated HUVECs, Kindlin-2 and cortical actin dissociated from stable AJs and redistributed to r
131                                    In cells, actin dynamics are regulated by kinases, such as the LIM
132   We previously demonstrated formin-mediated actin dynamics at the rear of the invading cell as well
133         Numerous phosphoproteins involved in actin dynamics including Wiskott-Aldrich syndrome protei
134 RIAM/Lpd (MRL) adapter protein Lpd regulates actin dynamics through interactions with Scar/WAVE and E
135 ical models to investigate how regulation of actin dynamics within foot processes controls local morp
136 loops can amplify stochastic fluctuations in actin dynamics, often resulting in traveling waves of pr
137                                Smooth-muscle actin expression by stellate cells and CD34 expression b
138 ication via western blots indicates that the actin expression is the same across all conditions.
139 celerating actin treadmilling in filamentous actin (F-actin) in a nucleotide-state dependent manner.
140 f the contractile ring including filamentous actin (F-actin), myosin, and septins and in forming the
141                                              Actin filament assembly and disassembly are vital for ce
142 blished a kinetic model of Ena/VASP-mediated actin filament elongation.
143 actin-activated ATPase activity and in vitro actin filament motility.
144 owth, were also found to have less disrupted actin filament networks after 2,4-D exposure.
145      Competing models have been proposed for actin filament nucleation by the bacterial proteins VopL
146                                We quantified actin filament order in human cells using fluorescence p
147 verexpressing miR-1 have profound defects in actin filament organization that are partially rescued b
148 with specific tropomyosin isoforms generates actin filament populations with distinct functional prop
149 A) obstructs phagocytosis through disrupting actin filament regulation processes - inhibiting polymer
150 very of new actin subunits to the elongating actin filament.
151 nding the structural design and evolution of actin filaments and their function in motility and host
152  site of endocytosis and initiates a zone of actin filaments assembled by Arp2/3 complex.
153 city of other formins to nucleate and bundle actin filaments but is notably less effective at process
154               Although the reorganisation of actin filaments during stomatal closure is documented, t
155                           Formins polymerize actin filaments for the cytokinetic contractile ring.
156                 Lamellipodia are networks of actin filaments generated and turned over by filament br
157        Here we demonstrate a liquid phase of actin filaments in the presence of the physiological cro
158 erved proteins that non-covalently crosslink actin filaments into tight bundles.
159 e tension generated by the E-cadherin/AmotL2/actin filaments plays a crucial role in developmental pr
160 geting drugs suggest that PMS contains short actin filaments that are depolymerization resistant and
161 model that enables simulation of networks of actin filaments, myosin motors, and cross-linking protei
162 all molecule inhibitor of drebrin binding to actin filaments, reduced the invasion of prostate cancer
163 ng and spreading cooperatively on individual actin filaments.
164 rsed migration mode characterized by dynamic actin-filled pseudopods that we call "alpha-motility." M
165  shape as they move, forming highly dynamic, actin-filled pseudopods.
166 E-activators of branched actin assembly-make actin-filled pseudopods.
167 s orient in the same direction as retrograde actin flow with their cytoskeleton-binding beta-subunits
168 RFYAASG-pen showed disruption of filamentous actin, focal adhesions and caveolae-mediated membrane tr
169 g the hMSC migration through mtROS-induced F-actin formation.
170                        Species with numerous actin genes are especially useful for the dissection of
171 are elevated in spines upon activity, with G-actin immobilized by the local enrichment of phosphatidy
172  the immunological synapse regulate cortical actin in CTLs, providing a potential mechanism through w
173 l morphology and disrupted organization of F-actin in Li1 plant cells by confocal microscopy.
174 ation in the back/side of the cell or with F-actin in the front of the cell.
175 g actin treadmilling in filamentous actin (F-actin) in a nucleotide-state dependent manner.
176                                OM slowed the actin-induced powerstroke, despite a twofold increase in
177 rmacophore of the key actin residues of Pfn1-actin interaction and therefore have the potential to ac
178 iological data suggest that multiple anillin-actin interaction modes promote the faithful progression
179 onstrate compound-induced inhibition of Pfn1-actin interaction.
180 evidence that the periodicity of subsynaptic actin is an important factor limiting the release of lar
181                  A similar reorganization of actin is induced by a constitutive dimer of MYO6+, indic
182      We found stimulated polymerization of F-actin is not required for Syk recruitment but is progres
183 necessarily weak binding of tropomyosin to F-actin is required for effective thin filament function.
184 cessity of minus-end-directed movement along actin is unclear as the underlying architecture of the l
185 ylnitrile; DCB), microtubules (oryzalin), or actin (latrunculin B).
186                   Although much of the basic actin machinery was intact, Cdc42 null cells lacked the
187 e that intermittent tethering of claudins to actin may allow for accommodation of the paracellular se
188                                Clathrin- and actin-mediated endocytosis is essential in eukaryotic ce
189 es bacteria from GBP encapsulation to resume actin-mediated motility and cell-to-cell spread.
190 roach to SMLM, in the context of the fibrous actin meshwork at the T cell immunological synapse, whos
191 n vitro and in vivo SHAPE-MaP for human beta-actin messenger RNA that revealed similar global folds i
192  Sertoli cell cytosol, causing truncation of actin microfilament, thereby failing to support the Sert
193 li cell injury through disruptive effects on actin microfilaments and microtubule (MT) organization a
194 Here we describe DeActs, genetically encoded actin-modifying polypeptides, which effectively induce a
195              Speed and space values of the F-actin molecular computers are discussed.
196  are especially useful for the dissection of actin molecular function due to redundancy and neofuncti
197  information processing capacity of a single actin molecule by calculating distributions of logical g
198               Moreover, we show that the two actin molecules in the unit cell are related to each oth
199 orders of magnitude higher than the in vitro actin monomer concentration required to support the obse
200                               They show that actin monomer levels are elevated in spines upon activit
201 e attenuated by increasing concentrations of actin monomers, suggesting competition between actin and
202 an mRNA-binding protein that transports beta-actin mRNA and releases it for local translation upon ph
203 tractile ring including filamentous actin (F-actin), myosin, and septins and in forming the subsequen
204 ular calcium concentration by disrupting the actin-myosin ATPase pathway.
205 istent with augmented steric-interference of actin-myosin binding.
206 to cell anchorage but instead is involved in actin network dynamics.
207 VirE2 protein can use the endogenous host ER/actin network for movement inside host cells.
208  as the underlying architecture of the local actin network is often unknown.
209 how that the retrograde flux of the branched actin network promotes the proximal growth of the FA and
210 for this cellular activity and regulation of actin network structure.
211 e parasite cytosol and labels an extensive F-actin network that connects parasites within the parasit
212 rowth and dynamically tethering the branched actin network to the WASP-family proteins that create it
213 on initiates by contraction of an equatorial actin network with randomly oriented filaments.
214 ay among membrane tension, the lamellipodial actin network, and adhesions coordinate the dynamics of
215 ns are known to promote assembly of branched actin networks by stimulating the filament-nucleating ac
216  TIRF microscopy of in vitro reconstituted F-actin networks, we observed and characterized two distin
217  to MT plus ends and cross-link the MT and F-actin networks.
218 ediated protrusion (via activation of Arp2/3 actin nucleation) and Rho-mediated contraction (via ROCK
219 NX9 activate N-WASP-WIP- and Arp2/3-mediated actin nucleation.
220                             We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD a
221 describe the interaction of myosin-5B with F-actin, nucleotides, and the pyrazolopyrimidine compound
222 ress without breaking in vitro compared with actin or microtubules, and also to increase cell elastic
223  for inhibiting junctional CDC-42 to control actin organization and AJ protein levels during epitheli
224 r3c1-dependent signaling and upregulation of actin-organizing molecules.
225  of gelsolin, without which abnormalities in actin polymerisation in the photoreceptor connecting cil
226  PAK1 signaling to N-WASP-cortactin-mediated actin polymerization and GLUT4 vesicle translocation.
227  to IL-20 that manifested as modification of actin polymerization and inhibition of a broad range of
228 letal organization by studying the effect of actin polymerization and nuclear rigidity on the diffusi
229 on of increased coat rigidity and force from actin polymerization enables robust vesiculation even at
230                  Whether talin ABDs regulate actin polymerization in a constitutive or regulated mann
231 ures that can mitigate the effect of Pfn1 on actin polymerization in vitro As a further proof-of-conc
232 of Arp3 (actin-related protein 3, a branched actin polymerization protein) and palladin (an actin bun
233 s in the model: substrate adhesion strength, actin polymerization rate, myosin contractility, and the
234 es microtubule organization as inhibition of actin polymerization with a low dose of latrunculin A di
235 from Tmods, acting as powerful nucleators of actin polymerization, not capping proteins.
236 that both proteins are involved in explosive actin polymerization, pseudopod formation, and cell migr
237 me, across multiple contexts, and depends on actin polymerization.
238                                              Actin polymerizes to form part of the cytoskeleton and o
239                  We further find that this G-actin pool functions in spine development and its modifi
240 lpha-positive cells, and alpha-smooth muscle actin-positive blood vessels were assayed at postoperati
241 abilizes filamentous actin without affecting actin protein expression and that GJA1-20k complexes wit
242 of the TJ-associated ZO-1 and cytoskeletal-F-actin proteins, correlated with modulation of hepatic ul
243 imed to identify small peptides arising from actin proteolysis, as influenced by the type of processi
244 tic viscosity-adhesion length, and a rate of actin protrusion.
245 d unloaded shortening velocity; (iii) myosin/actin ratio and myosin content in individual muscle fibr
246     IEC expulsion was accompanied by a major actin rearrangement in neighboring cells that maintained
247 croscopy to analyze nuclear morphology and F-actin rearrangements during the initiation, progression,
248 K activity was critical for ICAM-1-induced F-actin rearrangements.
249 opy, we now show that, after granule fusion, actin recovers at the synapse and no further secretion i
250               We also found that filamentous actin regulates microtubule organization as inhibition o
251 in as bait to recruit and phosphorylate host actin-regulating proteins.
252 , but rather is needed for proper junctional actin regulation during elongation.
253                        Here, we focus on the actin regulator Cortactin, a major organizer of protrusi
254 rulence factor IcsA, which recruits the host actin regulator N-WASP.
255                             Analyses with 11 actin regulators and three actin-targeting drugs suggest
256                     Among these targets were actin regulators, including the tumor suppressor eplin.
257 cally, PFOS caused mis-localization of Arp3 (actin-related protein 3, a branched actin polymerization
258  mutations in the ACTRT1 gene, which encodes actin-related protein T1 (ARP-T1), in two of the six fam
259 -beta insult caused cofilin activation and F-actin remodeling and decreased microtubule dynamics in t
260 unds that match the pharmacophore of the key actin residues of Pfn1-actin interaction and therefore h
261                     Lethal overexpression of actin results from mating this engineered strain with a
262 s fiber provides a traction force to promote actin retrograde flow and focal adhesion assembly.
263 cle myosin II bipolar filament assembly, and actin retrograde flow at the T-cell-substrate interface.
264 U251 glioma cell migration, morphology and F-actin retrograde flow rate can be shifted to lower stiff
265 cell communication involve the protrusion of actin-rich cell surface projections such as lamellipodia
266  VPR-1 promote mitochondrial localization to actin-rich I-bands in body wall muscle.
267                 Control of the dimensions of actin-rich processes like filopodia, lamellipodia, micro
268 d formation of putative podosome precursors: actin-rich puncta coinciding with matrix degradation sit
269 ion of the mouse orthologue of GPSM2 affects actin-rich stereocilia elongation in auditory and vestib
270                                              Actin's involvement in these processes is mediated by ma
271 rs of actin that stereo-specifically oxidize actin's M44 and M47 residues to induce cellular F-actin
272  subunits/s) disassembly, which depends on F-actin's nucleotide-bound state.
273 , that RPGR interacts with and activates the actin-severing protein gelsolin, and that gelsolin regul
274 a central component of the NPM-ALK-dependent actin signaling pathway.
275              In an attempt to identify novel actin signaling pathways regulated by NPM-ALK, a compreh
276        We demonstrate that OM can reduce the actin sliding velocity more than 100-fold in the in vitr
277 nvolved in an early, Rho family-independent, actin stabilization that is integral to the formation of
278 g the lesion exhibited increased filamentous actin staining, indicating active cell movement.
279 l velocity, induced elongation, and promoted actin stress fiber organization.
280                  Incorporation of NM-II into actin stress fiber provides a traction force to promote
281 sts to uniaxial cyclic stretch results in an actin stress fiber reinforcement response that stabilize
282  from stable AJs and redistributed to radial actin stress fibres of remodelling focal AJs.
283                2,4-D but not IAA altered the actin structure in long-term and short-term assays.
284                        Cb labels filamentous actin structures within the parasite cytosol and labels
285           Similar to other membrane-tethered actin structures, we find proteins localize in specific
286 a conformation clearly distinct from that of actin subunits in the helical filament.
287  1 domain, which facilitates delivery of new actin subunits to the elongating actin filament.
288 tin transport, on the other hand, is global: actin subunits typically diffuse across the entire lamel
289                 This direct interaction with actin suggests a new role of SPARC during tissue remodel
290  Analyses with 11 actin regulators and three actin-targeting drugs suggest that PMS contains short ac
291 re important post-translational effectors of actin that stereo-specifically oxidize actin's M44 and M
292                          In the absence of F-actin, the sperm DNA, centrioles, and organelles were tr
293                           Nesprin-2G engaged actin through its N terminus and microtubules through a
294 m, where a vinculin-dependent clutch couples actin to previously positioned adhesions.
295                               The diffusible actin transport, on the other hand, is global: actin sub
296 ys unique and essential role in accelerating actin treadmilling in filamentous actin (F-actin) in a n
297                 Energy landscapes based on F-actin-tropomyosin models show the mutation localizes tro
298  naturally leads to pattern transitions from actin vortices over stars into asters.
299                                  Tubulin and actin were apparently derived from bacterial precursors
300 s GJA1-20k expression stabilizes filamentous actin without affecting actin protein expression and tha

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