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1 step is covered by a diffusive search for an actin binding site.
2 n filaments, and kelch repeat 5 contains the actin binding site.
3 ds 391-404) is postulated to be an important actin binding site.
4 suggesting that the B subunit contained an F-actin binding site.
5 te, while the 50-20K loop (loop 2) is in the actin binding site.
6 etween the nucleotide binding pocket and the actin binding site.
7 tin by modulating the electric charge at the actin binding site.
8 myosin cross-bridges do not compete for an F-actin binding site.
9  the conformation and dynamics of the remote actin binding site.
10 end of the five-helix bundle distal from the actin binding site.
11 ing, suggesting that D6 contains a cryptic F-actin binding site.
12 led by the inability of the ELC to reach the actin-binding site.
13 ch Myo1b cross-links actin through a cryptic actin-binding site.
14 n filaments presumably by virtue of a second actin-binding site.
15 mic structure that, on average, has only one actin-binding site.
16 inase C, as well as a calcium/calmodulin and actin-binding site.
17 ication in the ring size does not change the actin-binding site.
18 n the acrosomal process implicate C837 at an actin-binding site.
19 stepping head while it searched for its next actin-binding site.
20 naling between the nucleotide pocket and the actin-binding site.
21  is lost when we remove the ESPN1 C terminus actin-binding site.
22  acid duplication, corresponding to a single actin-binding site.
23  is limited primarily by the availability of actin binding sites.
24                       EPLIN has at least two actin binding sites.
25 sequence have been proposed to correspond to actin binding sites.
26        We show that myosin-18A comprises two actin binding sites.
27 rary of drebrin deletion constructs to map F-actin binding sites.
28 e, and sterically eliminating one of these F-actin binding sites.
29 in (AC) family, apicomplexan ADFs lack key F-actin binding sites.
30 osed to correspond to seven quasi-equivalent actin binding sites.
31 tein structure, and subsequently disrupt the actin-binding sites.
32 hosphorylation site domain of MARCKS has two actin-binding sites.
33  UNC-60B might be involved in one of the two actin-binding sites.
34 d-tail interaction, unmasking its talin- and actin-binding sites.
35       They overlapped with the PIP2- but not actin-binding sites.
36 ound in pockets located within the two major actin-binding sites.
37 dicating these mutations include residues in actin-binding sites.
38 unication pathway between the nucleotide and actin-binding sites.
39 ces, which form three relatively independent actin-binding sites.
40  conformational change with full exposure of actin-binding site 1 could function as a switch mechanis
41        We document that exposure of a buried actin-binding site 1 in mutant alpha-actinin-4 causes an
42  increased by vinculin and depends mainly on actin-binding site 2 (ABS2) within the middle of the rod
43 atalytic head domain with an ATP-sensitive F-actin-binding site, a 3-kDa neck domain, which binds a s
44             The headpiece domain contains an actin-binding site, a cAMP-kinase phosphorylation site,
45  (aa1-76) in close proximity with the strong actin-binding site (aa193-254) in order to modulate the
46    A mutation, LK(47)/AA, within a predicted actin binding site (ABS) of F0 diminishes its interactio
47 hat the anillin ActBD harbors three distinct actin-binding sites (ABS 1-3).
48 rthermore, a mutation that ablates the first actin binding site (ABS1) in Actn4 abrogates the network
49                                        Three actin-binding sites (ABS1-3) have been reported: one in
50 ull cells, we show that while the C-terminal actin-binding site (ABS3) in talin is required for adhes
51 in activation, drebrin displacement from its actin-binding site, actin depolymerization/severing, and
52 olely by the arrangement of alpha-actinin to actin-binding sites along the axial filament.
53 trophin fragments corresponding to the novel actin binding site and the first 246 amino acids of dyst
54   The COOH-terminal region contains putative actin binding sites and a coiled-coil domain that mediat
55 ed by adjusting the spacing between adjacent actin binding sites and adjacent myosin heads in respons
56 s in which the spacing between both adjacent actin binding sites and adjacent myosin S1 heads changed
57 hanism (based on misregistration between the actin binding sites and the myosin cross-bridges) by whi
58 at N-terminal half of KLEIP, which lacks the actin-binding site and contains the sufficient sequence
59 nicate signals among the ATP-binding pocket, actin-binding site and the converter domain.
60 pathway between the nucleotide-binding site, actin-binding site and the converter domain.
61 ctA (residues 144-170) is C-terminal to both actin-binding sites and shares sequence homology with Ar
62 s a 139-amino-acid protein containing five F-actin-binding sites and two G-actin-binding sites, and i
63  lie in close proximity to the adjacent weak actin-binding sites and weak actomyosin ATPase inhibitor
64 o acid repeats are proposed to correspond to actin binding sites, and the middle periods are importan
65 orrelations among the nucleotide-pocket, the actin-binding site, and the converter; in kinesins, the
66 taining five F-actin-binding sites and two G-actin-binding sites, and interacts with wheat (Triticum
67 ence, apparently as a consequence of the two actin-binding sites, and is regulated by phosphorylation
68 hese lysines lie within previously predicted actin-binding sites, and the ASB2alpha-resistant filamin
69 ilin mutants with altered poly-L-proline and actin binding sites are discussed in the context of the
70 ules, provided both the Arp2/3 complex and F-actin binding sites are intact.
71 her than dimeric, implying that two distinct actin-binding sites are responsible for the actin-cross-
72 line the importance of filament geometry and actin binding site availability in quantitative theories
73  can bundle actin filaments using a single F-actin binding site, because it has the ability to self-a
74 he C terminus of domain III was the dominant actin-binding site both in vitro and in vivo.
75                              This additional actin-binding site bound to F-actin with a K(d) of appro
76                       Talin contains several actin binding sites, but we found that only the COOH-ter
77  at the end of the ATPase cycle disrupts the actin binding site by changing the conformation of the 5
78  myosin:ADP, both the catalytic site and the actin-binding site can each assume one of two conformati
79 Here, we show that fascin contains two major actin-binding sites, coinciding with regions of high seq
80                            The vinculin tail actin binding site comprises two distinct regions.
81 III spectrin, one of which overlaps with the actin-binding site conserved among spectrins.
82 hanges in the cofilin C-terminal filamentous actin binding site dependent on His133.
83 g the actomyosin interaction in myosin is an actin binding site distributed among several peptides on
84          Headpiece provides one of the two F-actin-binding sites essential for filament bundling.
85 tween the two propeller domains, leaving the actin binding sites exposed and flanking the cofilin bin
86 uggesting that, in addition to the two major actin-binding sites, fascin makes secondary contacts wit
87 y) N-terminal head domain with an ATPase and actin-binding site, followed by a neck domain to which t
88                 Schwannomin itself lacks the actin binding sites found in ezrin, radixin and moesin,
89 k growing filament barbed ends while three G-actin-binding sites (GABs) on other arms are available t
90                   Thus, the mutations in the actin binding site have little effect on ATP binding or
91 ntaining sequences homologous to caldesmon F-actin binding site I and II, respectively (CI, CII), bin
92                  Mutations in any one of the actin-binding sites impair the cellular function of fasc
93 nd spectrin has been well characterized, the actin binding site in 4.1R remains unidentified.
94           The partial accessibility of the F-actin binding site in the autoinhibited full-length vinc
95  domains and exposure of the high affinity F-actin binding site in the C-terminal domain.
96  directly bind to actin and contains a novel actin binding site in the center of the protein.
97     Motor activity is not essential, but the actin binding site in the head is important.
98 yosin IIIA that contains the ATP-independent actin binding site in the tail.
99 rminal domain of villin, is one of the two F-actin binding sites in villin necessary for F-actin bund
100 g sites were detected: a calcium-dependent G-actin-binding site in G1 and a calcium-independent G- an
101 ite in G1 and a calcium-independent G- and F-actin-binding site in G3 and G4.
102 ences unique to PKC betaII; thus defining an actin-binding site in PKC betaII that is not present in
103 etween the nucleotide-binding pocket and the actin-binding site in the lower 50-kDa domain (loop 2).
104 affinity appeared to be due to an additional actin-binding site in the N terminus of espin.
105            Only the mutants that retained an actin-binding site in the tail exhibited triphasic actin
106  by heavy chain phosphorylation (HCP) at the actin-binding site in vivo.
107 structural transition will destabilize the F-actin-binding sites in domain 2.
108 esized that the presence of two low-affinity actin-binding sites in dystrophin allows more elastic re
109 sis suggested that small espin contained two actin-binding sites in its COOH-terminal 116-amino acid
110 es: 1) there is a significant realignment of actin-binding sites in response to cross-bridge forces,
111 hrough three binding sites that overlap with actin-binding sites in villin.
112 hese exons are located in the Myo9b specific actin-binding site insert of the head domain and in the
113 at for S1 x MgATP the electric charge at the actin binding site is abolished.
114 e C-terminal subdomain suggest that the HP67 actin binding site is disrupted upon unfolding of the N-
115              Profilin with a mutation in its actin binding site is unable to rescue profilin RNAi, wh
116 ts N-terminal beta-propeller and a secondary actin binding site lies in a comparable location on its
117 p1p has two actin binding sites, the primary actin binding site lies on the edge of its N-terminal be
118 f these studies, our results suggest that an actin-binding site lies in the C-terminal domain of scru
119 lex digested with calpain revealed a novel F-actin binding site located near the middle of the dystro
120 , a major cardiac isoform, has an N-terminal actin-binding site located within residues 43-90.
121 our data suggest that a second, low affinity actin-binding site may be universally used by ADF/cofili
122 head of a stepping myosin V to find its next actin binding site more quickly, thus decreasing the pro
123  bundled by the peptide corresponding to the actin binding site of myristoylated alanine-rich protein
124 the headpiece fold and further defines the F-actin binding site of villin-type headpiece domains.
125 rded atomic resolution of the nucleotide and actin binding sites of the enzyme.
126 subunits with cofilin wedged between the two actin binding sites of the N- and C-terminal propeller d
127 terminal surface patch, overlapping with the actin-binding site of aldolase A and overlapping an area
128                               Mapping of the actin-binding site of Amot showed that serine 175 of Amo
129 t is part of the C-terminal tail domain, the actin-binding site of both isoforms.
130 P on actin also leads to an overlap with the actin-binding site of gelsolin domain I.
131  acid segment with a sequence similar to the actin-binding site of human profilin I was detected with
132 g motifs that are similar in sequence to the actin-binding site of mammalian profilin I.
133 omplex can be chemically cross-linked to the actin-binding site of profilin.
134     Furthermore, the P2 site in P2Ct and the actin-binding sites of Ct do not overlap, suggesting tha
135 nication pathway between the nucleotide- and actin-binding sites of myosin.
136                    Remarkably, the TRAP- and actin-binding sites of PfAldo seem to overlap, suggestin
137              An atomic homology model of the actin binding site on B2 was generated and molecular doc
138        One is analogous to the G-actin and F-actin binding site on cofilin, but we show using fluores
139         The other is analogous to a second F-actin binding site on cofilin, which in GMF appears to c
140 ) containing a sequence corresponding to the actin binding site on eNOS.
141 tryptophan were replaced with alanine in the actin binding site on eNOS.
142 tinct and separate, we propose that a second actin binding site on gelsolin competes with DNase I for
143                       Changing the number of actin binding sites on a WASP family protein, either by
144  that the orientation of postulated periodic actin binding sites on the coiled-coil surface is retain
145                             This exposes the actin-binding site on G4, enabling severing and capping
146  of S6 (including Pro-745) that contact an F-actin-binding site on S2 and buried F-actin-binding resi
147 th at least partial overlap of catalytic and actin-binding sites on aldolase.
148 nalling to the actin cytoskeleton occurs via actin-binding sites on betaII-spectrin.
149 F1alpha in mRNA targeting, we mapped the two actin-binding sites on EF1alpha at high resolution and d
150  of fascin indicate that there are two major actin-binding sites on fascin.
151 hat migrastatin analogues bind to one of the actin-binding sites on fascin.
152 t chain binding-domain, and the way that the actin-binding sites on myosin are arrayed around the act
153  form to a more open form in which the three actin-binding sites (on the G1, G2, and G4 subdomains) b
154  mutants, we verified that dematin has two F-actin binding sites, one in the core domain and the othe
155 1 surfaces, we identify two well-separated F-actin-binding sites, one of which contributes to actin f
156                          Mutations in Pfn1's actin-binding sites or reduction of Pfn1 eliminate the S
157 residue modules, each believed to contain an actin binding site, organized into seven-module superrep
158 ics and mutagenesis, we found that the EB1:F-actin binding site partially overlaps the well-character
159 n inside epithelial cells and bound to the F-actin-binding site region located in the carboxyl termin
160 in depolymerization activity, although the F-actin-binding sites remained exposed in the mutant G1-G3
161 RCKS may dimerize to form the two functional actin-binding sites requisite for cross-linking activity
162 ffect on actin networks, indicating that the actin binding sites reside probably exclusively within t
163                             In vinculin, the actin binding site resides in the tail domain.
164                                   The second actin-binding site resides in the generic motor domain a
165 1 amino acids in yeast, spanning from 7 to 4 actin binding sites respectively.
166                  Inactivation of this buried actin-binding site returns the affinity of the mutant to
167 ypothesized signaling pathway that links the actin-binding site's opening/closing with the nucleotide
168 Abp1 involve actin filament binding, yet the actin binding site(s) on Abp1 have not been identified,
169 n proteins with F-actin indicates that the F-actin binding site(s) on vinculin are located between re
170 inked to an allosteric reorganization of the actin binding site(s), which alters the structural dynam
171    Moreover, CaD1-597, which lacks the major actin-binding site(s), did not inhibit actin-filament ve
172 ts demonstrate that, in addition to a strong actin-binding site sequence between residues 718-723, tw
173 r domain, which contains the nucleotide- and actin-binding sites, some differences include the length
174 es in vitro of myosins with mutations in the actin binding site suggest losses of important contacts
175  what specific conformational changes in the actin binding site take place on binding to actin, and h
176 binds calmodulin and creates two coordinated actin-binding sites that constrain the actomyosin intera
177 ow present evidence for the existence of two actin-binding sites that not only mutually compete but a
178 ted mutagenesis suggested that Aip1p has two actin binding sites, the primary actin binding site lies
179 in tuning the allosteric couplings among the actin-binding site, the nucleotide-binding site, and the
180 Tmods have alternating tropomyosin (TM)- and actin-binding sites (TMBS1, ABS1, TMBS2 and ABS2).
181 reas Tmods have alternating tropomyosin- and actin-binding sites (TMBS1, ABS1, TMBS2, ABS2), Lmods la
182 h, and comprise alternating tropomyosin- and actin-binding sites (TMBS1, ABS1, TMBS2, and ABS2).
183              Restoration of the C-terminal F-actin binding site to TgADF stabilized its interaction w
184 of the B subunits of V-ATPase, we mapped the actin-binding site to a 44-amino acid domain.
185                        A comparison of their actin-binding site to macrolides found in the trisoxazol
186 o the mechanical strain propagating from the actin-binding site to the lever arm.
187                           We have mapped the actin-binding site to this surface and shown that helix
188  a 33-kDa intracellular protein with an avid actin-binding site, to the incubations resulted in a sup
189                                          The actin-binding site was mapped to a 10-residue region of
190 m a removal of steric hindrance blocking the actin-binding sites, we simulate with MD the stretching
191                               Three distinct actin binding sites were identified using a synthetic pe
192                                 At least two actin-binding sites were detected: a calcium-dependent G
193                                      Three F-actin-binding sites were mapped to sequences within amin
194 s a widely expressed protein that employs an actin-binding site with two calponin homology domains to
195                         Leiomodin shared two actin-binding sites with the filament pointed end-cappin
196 r(239) at the carboxyl-terminal end of the G-actin binding site, with some contribution by phosphoryl
197              We further find that a proposed actin-binding site within the missing connecting region
198 ded protein that contains well characterized actin-binding sites within the phosphorylation site doma

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