ライフサイエンスコーパス: cofilin 1

1 had abnormally high levels of phosphorylated cofilin-1.

2 one of the major actin-regulating proteins, cofilin-1.

3 ve also defined in the actin-binding protein cofilin-1 a link between PP2A, actin cytoskeleton, and n

4 Our study also identifies cofilin-1, a known regulator of actin dynamics, as a det

5 erization and severing, we hypothesized that cofilin-1 activity is regulated by Nephrin and is necess

6 One of the proteins identified was cofilin-1, an actin depolymerizing factor which regulate

7 Here, we show a central role of cofilin-1, an actin-binding protein that promotes actin

8 on of MRTF-A import occurs via activation of cofilin 1 and inactivation of vasodilator-stimulated pho

9 ember of the AC protein family that includes cofilin-1 and destrin, is predominantly expressed at sar

10 mpanied by activation (dephosphorylation) of cofilin-1 and its translocation to the F-actin rings.

11 gulated by Rho GTPases through Rho-Rock-Limk-Cofilin-1 and Rac/Cdc42-Pak-Limk-Cofilin-1 pathways.

12 he neural gene expression pattern of LIMK-1, cofilin-1, and beta-actin in all the experimental groups

13 protein levels of LIMK-1, cofilin-1, phospho-cofilin-1, and beta-actin in the whole brain lysates as

14 ance of actin dynamics through regulation of cofilin-1, and in executing learning and memory function

15 three focal proteins: vimentin, stathmin and cofilin-1, belonging to or involved in cytoskeletal orga

16 Additionally, cofilin-1, but not ADF, depletion increased epithelial p

17 Knockdown of either ADF or cofilin-1 by RNA interference increased the paracellular

18 The actin filament severing protein cofilin-1 (CFL-1) is required for actin and P-type ATPas

19 Here, we show that cofilin 1 (Cfl1), an actin-severing protein, and Vangl2,

20 mutants that lack the actin-severing protein cofilin 1 (CFL1).

21 2-fold), cyclophilin A (PPIA; 0.9-fold), and cofilin-1 (CFL1, 1.3-fold).

22 Here we determine the LIMK1:cofilin-1 co-crystal structure.

23 Similarly, constitutively inactive mutant of cofilin-1 (Cof1-S3D), known to stabilize the actin cytos

24 Mechanisms of such reorganization involve cofilin-1-dependent depolymerization and Arp2/3-assisted

25 The cofilin-1-dependent pathway affects the production of in

26 In a similar fashion, cofilin-1 dephosphorylation was observed in a rat model

27 The effect of cofilin-1 depletion on NF-kappaB activity and ICAM-1 exp

28 Loss of either ADF or cofilin-1 did not affect the steady-state morphology of

29 correlated with normal developmental loss of cofilin-1 expression within myofibers, suggesting that c

30 findings demonstrate novel roles for ADF and cofilin-1 in regulating the remodeling and permeability

31 We examined the roles of ADF and cofilin-1 in regulating the structure and functions of A

32 To investigate the necessity of cofilin-1 in the glomerulus, podocyte-specific Cfl1 null

33 We conclude that cofilin-1 is necessary for maintenance of normal podocyt

34 Phosphorylation of cofilin-1 is regulated by Rho GTPases through Rho-Rock-L

35 wild type cofilin-1 or constitutively active cofilin-1 mutant (Cof1-S3A), known to destabilize the ac

36 Together, these data show that cofilin-1 occupies a central position in RhoA-actin path

37 Overexpression of wild type cofilin-1 or constitutively active cofilin-1 mutant (Cof

38 ronal morphology and dysregulation of LIMK-1/cofilin-1 pathway could affect the cognitive outcome aft

39 o-Rock-Limk-Cofilin-1 and Rac/Cdc42-Pak-Limk-Cofilin-1 pathways.

40 ed with diminished protein levels of LIMK-1, cofilin-1, phospho-cofilin-1, and beta-actin in the whol

41 BIG2 siRNA, levels of cytosolic Arp2, Arp3, cofilin-1, phosphocofilin, vinculin, and Grb2, known to

42 can fully compensate for low levels of smn, cofilin 1, profilin 2 and alpha-actinin 1 did not affect

43 expression within myofibers, suggesting that cofilin-1 serves as an early developmental sarcomeric is

44 Cofilin-1-severing/depolymerization activity is negative

45 LIMK-1/cofilin-1 signaling pathway is known to be involved in t

46 RNA interference knockdown of cofilin-1 stabilized the actin filaments and inhibited t

47 Ezrin-dependent actin remodeling involved cofilin-1 that is essential for the turnover and reorgan

48 Additionally, depletion of cofilin-1 was associated with a marked reduction in ICAM

49 Differential expression of cofilin-1 was due to increased phosphorylation.

50 in either WT or cofilin-2-deficient muscles, cofilin-1 was similarly expressed in developing myofiber

51 Phosphorylated, inactive cofilin-1 was up-regulated in diabetic glomeruli, sugges

52 ripherin, vimentin, gamma-tropomyosin 3, and cofilin 1 were present in the axonal preparations.