ライフサイエンスコーパス: drebrin

1 -43 (GAP-43) and the dendritic spine marker, drebrin.

2 hat the spines contain filamentous actin and drebrin.

3 actin complex are identified as spectrin and drebrin.

4 that F-actin is stabilized by the binding of drebrin.

5 e actin-remodeling proteins Flightless-1 and Drebrin.

6 m loss of the spine actin-regulatory protein Drebrin.

7 its ADFH/linker domain that is not bound by drebrin.

8 h was associated with a decrease in cortical drebrin (-25%), but without enhancement of Abeta/tau pat

9 ment in the proportion of spines labeled for drebrin A and no significant change in spine density at

10 We sought to determine whether drebrin A arrives at the plasma membrane of neurons, in

11 d beyond for both genotypes, suggesting that drebrin A confers stability to postsynaptic spines.

12 Western blotting showed that drebrin A emerges at postnatal day (PNd) 6 and becomes p

13 x of 2xKI mice, in which synapse density and drebrin A immunoreactivity levels remain unchanged at 6

14 At PNd7, patches of drebrin A immunoreactivity were discretely localized to

15 highly significant reduction in the level of drebrin A immunoreactivity within each spine.

16 nths and older, a larger fraction of spinous drebrin A in 2xKI mice was located near the synaptic mem

17 this end, a new antibody was used to locate drebrin A in relation to electron microscopically imaged

18 , consistently supporting the involvement of drebrin A in spinogenesis and synaptogenesis.

19 ght microscopy showed high concentrations of drebrin A in the synaptic layers of the hippocampus and

20 Electron microscopy revealed that drebrin A in these regions is located exclusively in den

21 Drebrin A is a neuron-specific, actin binding protein.

22 Drebrin A is one protein reported to modulate spine size

23 esumably excitatory) synapses and containing drebrin A is reduced and if so, whether this occurs prio

24 proportion of hippocampal spines containing drebrin A is reduced and this change is accompanied by a

25 These findings indicate that drebrin A is required for the rapid (<30 minutes) form o

26 In adulthood, nearly all of the synaptic drebrin A is within spines forming asymmetric excitatory

27 Thus, drebrin A may be involved in organizing the dendritic po

28 s, soluble Abeta could affect spines lacking drebrin A more strongly than spines containing drebrin A

29 creased levels of synaptophysin, PSD-95, and drebrin A protein levels.

30 The drebrin A sites exhibited only thin postsynaptic densiti

31 al density of postsynaptic spines containing drebrin A was relatively constant from 3 to 18 months an

32 Thus, we examined levels of drebrin A within postsynaptic spines in the hippocampus

33 , the proportion of postsynaptic spines with drebrin A within somatosensory cortex layer I was smalle

34 Drebrin A, an actin-binding protein, is a key regulatory

35 thood depends on an F-actin binding protein, drebrin A, mice deleted of the adult isoform of drebrin

36 nts confirmed that the reduced proportion of drebrin A-containing spines in brains of FAD mice at 6 m

37 ebrin A more strongly than spines containing drebrin A.

38 and areal density of spine profiles lacking drebrin A.

39 Finally, we show that drebrin, a protein known to mediate interactions between

40 overed two domains in the N-terminal half of drebrin-a coiled-coil domain and a helical domain-that i

41 construct that competes with EB3 binding to drebrin, also inhibited invasion of prostate cancer cell

42 mer's disease (AD) exhibit reduced levels of drebrin, an F-actin binding protein of dendritic spines

43 Drebrin and alpha-actinin-2, actin-binding proteins conc

44 ween Abeta*56 and two postsynaptic proteins (drebrin and fyn kinase), but none between amyloid-beta d

45 ation of RNAi-based inhibition of endogenous drebrin and GFP-tagged expression of wild-type and mutan

46 Full-length drebrin and its C-terminal truncated constructs were use

47 and charged/helical actin binding domains of drebrin and mAbp1 are sufficient for regulated binding t

48 gy through two shared actin binding domains, drebrin and mAbp1 have different subcellular localizatio

49 Drebrin and mammalian Abp1 (mAbp1) are actin-binding pro

50 Unexpectedly, actin and the actin regulators drebrin and myosin 6 mediate ectosome release from the t

51 the previously observed competition between drebrin and several other F-actin-binding proteins.

52 of wild-type and mutant forms, we establish drebrin as a negative regulator of HIV entry and HIV-med

53 in and microtubule activity, and we identify drebrin as a potential coordinator of these cytoskeletal

54 ly identified the actin reorganizing protein Drebrin as a target of the immunosuppressant 3,5-bistrif

55 stribute with the actin-associated component drebrin, as do the clusters on ciliary ganglion neurons,

56 nd the postsynaptic actin-regulating protein drebrin, as in AD brain.

57 We show that drebrin associates with CXCR4 before and during HIV infe

58 ay using BTP2, a small molecule inhibitor of drebrin binding to actin filaments, reduced the invasion

59 Understanding how drebrin binds and remodels F-actin is important for a fu

60 After viral internalization, drebrin clustering is retained in a fraction of the inte

61 These findings show that drebrin contains a cryptic F-actin-bundling activity reg

62 Drebrin couples dynamic microtubules to F-actin in growt

63 brin A, mice deleted of the adult isoform of drebrin (DAKO) but retaining the embryonic isoform (dreb

64 s the postsynaptic actin stabilising protein Drebrin (DBN).

65 The actin binding domain of drebrin decreases the intrastrand disulfide cross-linkin

66 llular and in vitro assays with a library of drebrin deletion constructs to map F-actin binding sites

67 Functional perturbations of drebrin demonstrate that proximal leading process microt

68 function in PAK leads to cofilin activation, drebrin displacement from its actin-binding site, actin

69 udies identified the actin-binding domain of drebrin (DrABD), which causes the same rearrangements in

70 citatory synapses of adult cortices, whereas drebrin E is sufficient for maintaining basal NR2A level

71 (DAKO) but retaining the embryonic isoform (drebrin E) were generated.

72 amic microtubules and actin filaments by the drebrin/EB3 pathway drives prostate cancer cell invasion

73 Disruption of the drebrin/EB3 pathway using BTP2, a small molecule inhibit

74 We show here that the drebrin/EB3 pathway, which co-ordinates dynamic microtub

75 Drebrin expression is restricted to basal epithelial cel

76 Down-regulation of drebrin expression promotes HIV-1 entry, decreases F-act

77 y, the Siah2 E3 ubiquitin ligase antagonizes drebrin function, suggesting a model for control of the

78 and EM, the rescue of filament formation by drebrin in different cases of longitudinal interprotomer

79 These data underscore the negative role of drebrin in HIV infection by modulating viral entry, main

80 , we analyze the role of the actin modulator drebrin in HIV-1 viral infection and cell to cell fusion

81 I3K, GSK-3beta, tau, MAP2, synaptophysin and drebrin in the lumbar spinal cord of non-diabetic and st

82 d the S100B animals, the immunoreactivity of drebrin increased with age, however there were no signif

83 Drebrin inhibits depolymerization mainly at the barbed e

84 Precisely how drebrin interacts with F-actin and how this is regulated

85 s nanoscale architecture wherein f-actin and drebrin intervene between microtubules and the plasma me

86 Drebrin is a filament-binding protein involved in organi

87 Drebrin is a mammalian neuronal protein that binds to an

88 We show that drebrin is a specific component of the cytochalasin D-se

89 Drebrin is actively recruited toward cell-virus and Env-

90 Drebrin is also upregulated in human prostate cancer cel

91 Drebrin is an actin filament (F-actin)-binding protein w

92 n protomer 1 and that native cysteine 308 of drebrin is near C374 of actin protomer 2.

93 ich localize to the Golgi apparatus, but not drebrin, is blocked by occupation of the p23 cargo-prote

94 the 3' untranslated regions (UTRs) of DBNL (drebrin-like protein) and TACC1 (transforming acidic coi

95 Drebrin localization to the cell surface was found to in

96 fficient to cause similar cofilin pathology, drebrin loss and memory impairment, consistent with a po

97 ectly involved in PAK signaling deficits and drebrin loss in Abeta oligomer-treated hippocampal neuro

98 elease and passive systemic anaphylaxis, and Drebrin(-/-) mast cells also exhibit defects in Fcepsilo

99 Drebrin(-/-) mast cells exhibit defects in actin cytoske

100 In this study, we show that Drebrin(-/-) mice exhibit reduced IgE-mediated histamine

101 By using the drebrin microtubule-actin crosslinking protein as an ent

102 Here, the structural effects of drebrin on F-actin were examined in solution.

103 Furthermore, gain- or loss-of-function of drebrin or EB3 by over-expression or siRNA-mediated knoc

104 Our results indicate that Drebrin regulates the actin cytoskeleton and calcium res

105 Additionally, we show that drebrin rescues the polymerization of V266G/L267G, a hyd

106 Efficient cross-linking of drebrin residues 238, 248, 252, 270, and 271 to actin re

107 the actin-binding proteins mAbp1 (SH3p7) and drebrin share sequence homology, they are differentially

108 Overall, our data suggest that drebrin stabilizes actin filaments through its effect on

109 tin and observe the binding cooperativity of drebrin to F-actin with nanometer resolution.

110 nisms for selective recruitment of mAbp1 and drebrin to Golgi membranes indicate how actin-based stru

111 tant proteins and chimeras between mAbp1 and drebrin to identify motifs that direct targeting.

112 sed levels of the spine cytoskeletal protein drebrin, was blocked by the Alzheimer's therapeutic drug

113 creased, and expression of synaptophysin and drebrin were reduced in diabetic rats.

114 m loss of the spine actin-regulatory protein drebrin, which cofilin removes from actin.