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1  the repeat domain maintains a significant F-actin binding activity.
2 in binding domains and lead to a decrease in actin binding activity.
3 dystrophin, utrophin, shared this rod domain actin binding activity.
4 tic activity, D33S (Asp --> Ser), had normal actin binding activity.
5 utant, K229A (Lys --> Ala), had intermediate actin binding activity.
6 hat serine 175 of Amot was important for the actin-binding activity.
7 ons on both protein aggregation and impaired actin-binding activity.
8 irst 20 amino acids of the latter exposes an actin-binding activity.
9 gment of villin that retains strong in vitro actin-binding activity.
10 CKS are necessary and sufficient to regulate actin-binding activity.
11 vailability of the PSD so as to activate its actin-binding activity.
12  (W59R and I149del) also showed an increased actin-binding activity.
13 found to contribute to the regulation of its actin-binding activity.
14 ins was previously shown to be necessary for actin-binding activity.
15 f a GRE reporter while still maintaining its actin-binding activity.
16 nphosphorylated UtrN-R3 without altering its actin-binding activity.
17  CapZbeta proteins, and this domain displays actin-binding activity.
18 y mechanism dependent on both motor and tail actin-binding activity [1].
19 ked ACTN4 mutant, K255E, which has increased actin binding activity and is predominantly cytoplasmic,
20                   This requires profilin's G-actin binding activity and its direct interaction with H
21 role of the first repeat of beta-spectrin in actin binding activity and of the second repeat in assoc
22          Biochemically, we characterize FRG1 actin binding activity and show that the cytoplasmic poo
23 l glomerulosclerosis) demonstrated increased actin binding activity and susceptibility of ACTN4 to ca
24 f human gelsolin domain 2 were assayed for F-actin binding activity and thermodynamic stability.
25  We show that myosin IIIB (MYO3B) lacks tail actin-binding activity and is unable to target COS7 cell
26  elegans HMP-1/alpha-catenin regulates its F-actin-binding activity and organization of junctional-pr
27 ins that requires both motor and tail domain actin-binding activity and show that the actin-binding t
28 outer membrane protein(s) with ATP-sensitive actin binding activity, and (2) a salt-inextractable, pr
29 eracts strongly with PPIs, and its monomeric actin-binding activity becomes regulated by PPIs.
30  A or truncation by mutagenesis eliminated F-actin binding activity but strongly enhanced actin depol
31 differences that account for their different actin-binding activities could not be determined.
32 iece have been purified and tested for their actin binding activity, cysteine reactivity, and thermal
33  of FSGS ACTN4 mutants to downregulate their actin binding activities for ameliorating the glomerulos
34  with chimeric proteins demonstrate that the actin binding activity fully correlates with the ability
35 lear function of ACTN4 is independent of its actin binding activity in the cytoplasm.
36 artitioning of eEF-1A in Triton X-114 or its actin-binding activity in in vitro assays.
37                   We have identified a novel actin-binding activity in the polyproline domain of both
38                     The significance of CP's actin-binding activity in vivo was tested by determining
39 unlike known actin-binding proteins, SHTN1's actin binding activity is intrinsically inhibited by a p
40 acterize a point mutant, H41F, which retains actin-binding activity, is more thermostable but, intere
41 E), or a protein fraction with ATP-sensitive actin-binding activity isolated from SE, to salt-washed
42 es not contain VI and VII regions, retains F-actin binding activity, its binding affinity for F-actin
43 S-transferase fusion proteins demonstrate an actin-binding activity mediated specifically by the kelc
44                                          The actin binding activities of the B subunits of V-ATPase r
45 These results suggest that EGF regulates the actin binding activity of ACTN4 by inducing tyrosyl-dire
46  of cortactin, which, in turn, changes the F-actin binding activity of cortactin.
47 ition, pp60(c-src) moderately inhibits the F-actin binding activity of cortactin.
48              We queried whether the elevated actin binding activity of FSGS mutants can be downregula
49 utive spectrin-like repeats recapitulate the actin binding activity of full-length utrophin more fait
50 of gelsolin-LPS binding is inhibition of the actin binding activity of gelsolin as well as the actin
51 ver, overexpression of NtRac1 diminishes the actin binding activity of green fluorescent protein (GFP
52 lture cell caldesmon and tropomyosin (TM) on actin binding activity of human fascin.
53                     It is thought that the F-actin binding activity of IQGAP1 is regulated by its rev
54  found that Y4/31E significantly reduced the actin binding activity of K255E, T259I and S262P, dramat
55 ts and actin filaments may contribute to the actin binding activity of other members of the actin cro
56 st for possible physiologic functions of the actin binding activity of V-ATPase, early responses of r
57 t the Hippo pathway negatively regulates the actin-binding activity of Amot family members through di
58 large multidomain proteins that regulate the actin-binding activity of capping protein (CP), a major
59        The interaction with PA inhibited the actin-binding activity of CP.
60                                          The actin-binding activity of fascin is down-regulated by ph
61 ses and the actin cytoskeleton, and that the actin-binding activity of IQGAP1 is regulated by calmodu
62           These substitutions eliminated the actin-binding activity of the B subunit fusion proteins.
63                                        The F-actin-binding activity of unacetylated Tpm1p is reduced
64                                          The actin-binding activity of vinculin is inhibited by an in
65 e results demonstrate that activation of the actin-binding activity of vinculin requires steps other
66 al third of dystrophin displayed no specific actin binding activity or competition with full-length d
67 > Ala), and R148A (Arg --> Ala), had minimal actin binding activity relative to wild type (wt) aldola
68 625-MDE exhibited actin-activated ATPase and actin-binding activities similar to wild-type MDE.
69 n-type headpiece domain natively devoid of F-actin binding activity, that of supervillin headpiece (S
70 lding of the N-terminal domain which confers actin-binding activity to villin-type headpiece domains,
71 issense mutations cause disease by impairing actin-binding activity, we engineered the K18N, L54R, D1
72 regulated kinase 1a negatively regulates its actin-binding activity without significantly affecting i