ライフサイエンスコーパス: drebrin

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

2 -43 (GAP-43) and the dendritic spine marker, drebrin.

3 hat the spines contain filamentous actin and drebrin.

4 actin complex are identified as spectrin and drebrin.

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

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

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

8 n in cultured podocytes via interaction with Drebrin-1.

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

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

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

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

13 We found that neuronal drebrin A directly interacts with mDia2 formin.

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

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

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

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

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

19 We hypothesize that accumulation of drebrin A in DS (that coincides with spine maturation) l

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

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

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

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

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

25 Neuron-specific drebrin A is highly enriched in dendritic spines (postsy

26 Drebrin A is one protein reported to modulate spine size

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

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

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

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

31 uggesting that neuron-specific actin-binding drebrin A may be a part of such a switch.

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

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

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

35 The drebrin A sites exhibited only thin postsynaptic densiti

36 d an array of synthetic peptides of neuronal drebrin A to map its formin-binding interface.

37 Drebrin A was previously shown to inhibit actin nucleati

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

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

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

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

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

43 ll documented that DS are highly enriched in drebrin A, which is critical for their plasticity and fu

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

45 ebrin A more strongly than spines containing drebrin A.

46 and areal density of spine profiles lacking drebrin A.

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

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

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

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

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

52 nteraction highlighted binding sites between drebrin and crystallized CXCR4.

53 co-IP confirmed a direct interaction between drebrin and CXCR4 in PN4 hippocampi.

54 o-IP) confirmed a direct interaction between drebrin and CXCR4 using wild-type E14.5 whole head and a

55 Drebrin and formins are key regulators of neuronal actin

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

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

58 d stabilizes them, but the interplay between drebrin and INF2 on actin filament stabilization is not

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

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

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

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

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

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

65 iction then identified binding sites between drebrin and the microtubule plus end protein, EB1, and s

66 of other synaptic proteins, such as PSD-95, drebrin, and homer1, remained unchanged in the parietote

67 ese findings establish an essential role for drebrin, and upstream transcriptional regulator HDAC2, i

68 INF2 and drebrin are abundantly expressed in highly specialized c

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

70 e of the dendritic spine scaffolding protein Drebrin as a pathophysiologically relevant autoantibody

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

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

73 otting, for which mass spectrometry revealed Drebrin as the putative antigen.

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

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

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

77 Anti-Drebrin autoantibodies define a chronic syndrome of recu

78 osure of primary hippocampal neurons to anti-Drebrin autoantibodies resulted in aberrant synapse comp

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

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

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

82 lution microscopy revealed decreased EB1 and drebrin coexpression after drebrin inhibition.

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

84 Drebrin couples dynamic microtubules to F-actin in growt

85 In migrating GnRH neurons, drebrin, CXCR4, and the microtubule plus-end binding pro

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

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

88 a role for the cytoskeletal binding protein drebrin (Dbn1) in regulating Layer II/III cortical proje

89 Here, we show that the cytoskeletal protein drebrin (Dbn1) regulates excitatory Layer II/III cortica

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

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

92 Functional perturbations of drebrin demonstrate that proximal leading process microt

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

94 resulted in aberrant synapse composition and Drebrin distribution as well as increased spike rates an

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

96 Notably, truncated drebrin - DrbA1-300 - is sufficient for this protection,

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

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

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

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

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

102 primary neurons established that inhibiting drebrin (either pharmacologically or using cells from DB

103 Drebrin expression is restricted to basal epithelial cel

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

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

106 Deletion of the C-terminal region of drebrin greatly reduces its binding to mDia2 and the ext

107 Decreased levels of drebrin in dendritic spines is a hallmark of Alzheimer's

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

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

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

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

112 gatively regulates the actin-binding protein drebrin in the NAc.

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

114 decreased EB1 and drebrin coexpression after drebrin inhibition.

115 Drebrin inhibits depolymerization mainly at the barbed e

116 Drebrin inhibits formin-mediated nucleation of actin and

117 molecular level understanding of the formin-drebrin interaction and will help to unravel its biologi

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

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

120 Drebrin is a filament-binding protein involved in organi

121 Drebrin is a mammalian neuronal protein that binds to an

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

123 rmins from different subfamilies showed that drebrin is a specific rather than general inhibitor of t

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

125 Drebrin is also upregulated in human prostate cancer cel

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

127 Drebrin is another actin-binding protein that also binds

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

129 olecular binding interface between mDia2 and drebrin is necessary to better understand the functional

130 We demonstrate that drebrin is transcriptionally repressed by the histone mo

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

132 nd increase dendritic spine density, whereas drebrin knockdown potentiates these effects.

133 Analysis of drebrin knockout (DBN1 KO) mice showed delayed migration

134 unohistochemistry in brains of wild-type and Drebrin knockout mice to in vitro analyses of impaired s

135 nin-dependent interaction of N-cadherin with Drebrin-like (Dbnl), an actin-binding protein that is in

136 In brief, we demonstrate that Dbnl and Drebrin-like B-catenin assist in the maturation of pro-N

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

138 Drebrin localization to the cell surface was found to in

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

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

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

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

143 ts we identified the domain requirements for drebrin-mDia2 interaction.

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

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

146 oth N-terminal and C-terminal regions of the drebrin molecule.

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

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

149 g virus-mediated gene transfer, we show that drebrin overexpression in the NAc is sufficient to decre

150 und 70kDa on Western blotting were also anti-Drebrin-positive.

151 fluorescence microscopy imaging to show that drebrin protects actin filaments from severing by INF2 w

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

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

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

155 vealed T-lymphocytic encephalitis in an anti-Drebrin-seropositive patient.

156 tent in cerebrospinal fluid occurred in anti-Drebrin-seropositive patients.

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

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

159 Developmentally regulated brain protein (drebrin) stabilizes actin polymerization, interacts with

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

161 CXCR4 under SDF-1 stimulation interacts with drebrin to facilitate neuronal migration.

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

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

164 The mDia2-interacting interface on drebrin was narrowed down to three highly conserved 9-16

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

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

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

168 a multi-pronged interface between mDia2 and drebrin, which involves both N-terminal and C-terminal r