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1 had abnormally high levels of phosphorylated cofilin-1.
2  one of the major actin-regulating proteins, cofilin-1.
3 sociation of the E1 enzyme to the substrate, cofilin-1.
4 -amino group as the SUMO-conjugation site of cofilin-1.
5 ve also defined in the actin-binding protein cofilin-1 a link between PP2A, actin cytoskeleton, and n
6                    Our study also identifies cofilin-1, a known regulator of actin dynamics, as a det
7 erization and severing, we hypothesized that cofilin-1 activity is regulated by Nephrin and is necess
8           One of the proteins identified was cofilin-1, an actin depolymerizing factor which regulate
9              Here, we show a central role of cofilin-1, an actin-binding protein that promotes actin
10 on of MRTF-A import occurs via activation of cofilin 1 and inactivation of vasodilator-stimulated pho
11        Using RNAi, we find that co-depleting cofilin-1 and actin depolymerizing factor (ADF) led to a
12            Collectively, our data identifies cofilin-1 and ADF as actin remodeling factors required f
13                    Strikingly, cells without cofilin-1 and ADF had blebs with abnormally long necks.
14 riched at leader bleb necks, whereas RNAi of cofilin-1 and ADF reduced bleb sizes and the frequency o
15 ember of the AC protein family that includes cofilin-1 and destrin, is predominantly expressed at sar
16  to the AC group of proteins, which includes cofilin-1 and destrin.
17 mpanied by activation (dephosphorylation) of cofilin-1 and its translocation to the F-actin rings.
18 gulated by Rho GTPases through Rho-Rock-Limk-Cofilin-1 and Rac/Cdc42-Pak-Limk-Cofilin-1 pathways.
19 he neural gene expression pattern of LIMK-1, cofilin-1, and beta-actin in all the experimental groups
20 protein levels of LIMK-1, cofilin-1, phospho-cofilin-1, and beta-actin in the whole brain lysates as
21 ed alpha-enolase, 14-3-3 protein zeta/delta, cofilin-1, and heat shock cognate 71 kDa protein as nove
22 of alpha-enolase, 14-3-3 protein zeta/delta, cofilin-1, and heat shock cognate 71 kDa protein into a
23 ance of actin dynamics through regulation of cofilin-1, and in executing learning and memory function
24 three focal proteins: vimentin, stathmin and cofilin-1, belonging to or involved in cytoskeletal orga
25 e show that the N-alpha-SUMOylation promotes cofilin-1 binding to F-actin and cofilin-induced actin d
26                             However, RNAi of cofilin-1 but not ADF led to a significant decrease in c
27                                Additionally, cofilin-1, but not ADF, depletion increased epithelial p
28                   Knockdown of either ADF or cofilin-1 by RNA interference increased the paracellular
29          The actin filament severing protein cofilin-1 (CFL-1) is required for actin and P-type ATPas
30 ther NUDC interacts with the actin modulator cofilin 1 (CFL1) and found that in rods, CFL1 is localiz
31 sed gene expression of actin-binding protein cofilin 1 (CFL1) in endocervix in the E2-dominated proli
32                           Here, we show that cofilin 1 (Cfl1), an actin-severing protein, and Vangl2,
33 mutants that lack the actin-severing protein cofilin 1 (CFL1).
34 2-fold), cyclophilin A (PPIA; 0.9-fold), and cofilin-1 (CFL1, 1.3-fold).
35                  Here we determine the LIMK1:cofilin-1 co-crystal structure.
36 Similarly, constitutively inactive mutant of cofilin-1 (Cof1-S3D), known to stabilize the actin cytos
37 oss of the F-actin-severing proteins ADF and cofilin-1 decreased barbed end availability at stereocil
38    Mechanisms of such reorganization involve cofilin-1-dependent depolymerization and Arp2/3-assisted
39                                          The cofilin-1-dependent pathway affects the production of in
40                        In a similar fashion, cofilin-1 dephosphorylation was observed in a rat model
41                                The effect of cofilin-1 depletion on NF-kappaB activity and ICAM-1 exp
42                        Loss of either ADF or cofilin-1 did not affect the steady-state morphology of
43 correlated with normal developmental loss of cofilin-1 expression within myofibers, suggesting that c
44 ysine(s), serves as an essential PTM to tune cofilin-1 function during regulation of actin dynamics.
45 findings demonstrate novel roles for ADF and cofilin-1 in regulating the remodeling and permeability
46             We examined the roles of ADF and cofilin-1 in regulating the structure and functions of A
47              To investigate the necessity of cofilin-1 in the glomerulus, podocyte-specific Cfl1 null
48 MOylation is that the N-alpha-SUMOylation of cofilin-1 is also mediated by SUMO activating (E1), conj
49                           Here, we show that cofilin-1 is conjugated by SUMO1 both in vitro and in vi
50                  In support of this concept, cofilin-1 is found to localize to a single cell edge.
51                             We conclude that cofilin-1 is necessary for maintenance of normal podocyt
52                           Phosphorylation of cofilin-1 is regulated by Rho GTPases through Rho-Rock-L
53 wild type cofilin-1 or constitutively active cofilin-1 mutant (Cof1-S3A), known to destabilize the ac
54               Together, these data show that cofilin-1 occupies a central position in RhoA-actin path
55                  Overexpression of wild type cofilin-1 or constitutively active cofilin-1 mutant (Cof
56 ronal morphology and dysregulation of LIMK-1/cofilin-1 pathway could affect the cognitive outcome aft
57 o-Rock-Limk-Cofilin-1 and Rac/Cdc42-Pak-Limk-Cofilin-1 pathways.
58 ed with diminished protein levels of LIMK-1, cofilin-1, phospho-cofilin-1, and beta-actin in the whol
59  BIG2 siRNA, levels of cytosolic Arp2, Arp3, cofilin-1, phosphocofilin, vinculin, and Grb2, known to
60  can fully compensate for low levels of smn, cofilin 1, profilin 2 and alpha-actinin 1 did not affect
61            It was previously documented that cofilin-1 promotes cortical actin turnover at leader ble
62          In monocytes, our data suggest that cofilin-1 promotes the local upregulation of myosin cont
63 gation by SUMO at the N-alpha amino group of cofilin-1, rather than at an internal lysine(s), serves
64 expression within myofibers, suggesting that cofilin-1 serves as an early developmental sarcomeric is
65                                              Cofilin-1-severing/depolymerization activity is negative
66                                       LIMK-1/cofilin-1 signaling pathway is known to be involved in t
67                RNA interference knockdown of cofilin-1 stabilized the actin filaments and inhibited t
68    Ezrin-dependent actin remodeling involved cofilin-1 that is essential for the turnover and reorgan
69                                     We found cofilin-1 to be enriched at leader bleb necks, whereas R
70                   Additionally, depletion of cofilin-1 was associated with a marked reduction in ICAM
71                   Differential expression of cofilin-1 was due to increased phosphorylation.
72 in either WT or cofilin-2-deficient muscles, cofilin-1 was similarly expressed in developing myofiber
73                     Phosphorylated, inactive cofilin-1 was up-regulated in diabetic glomeruli, sugges
74 ripherin, vimentin, gamma-tropomyosin 3, and cofilin 1 were present in the axonal preparations.