ライフサイエンスコーパス: VDAC1

1 VDAC1 and phosphate carrier protein are the first OMM pr

2 VDAC1 co-purifies with cholesterol and is functionally r

3 VDAC1 is overexpressed in post-mortem brains of Alzheime

4 VDAC1, ANT1, and HKII were present in the PKCepsilon com

5 VDAC1-based peptides interacted with Bcl2 to prevent its

6 VDAC1-DeltaC may also hold promise as a biomarker for tu

7 leased by voltage-dependent anion channel 1 (VDAC1) after sciatic nerve injury triggers Schwann cell

8 articular voltage-dependent anion channel 1 (VDAC1) and contactin-associated protein 1 (CNTNAP1), red

9 ) and the voltage-dependent anion channel 1 (VDAC1) at the outer mitochondrial membranes.

10 ession of voltage-dependent anion channel 1 (VDAC1) induced Parkin translocation to mitochondria, pre

11 e protein voltage-dependent anion channel 1 (VDAC1) is a convergence point for a variety of cell surv

12 ounded to voltage dependent anion channel 1 (VDAC1) on the mitochondrial outer membrane and inhibited

13 acts with voltage-dependent anion channel 1 (VDAC1) on the OMM, which then facilitates processing of

14 ession of voltage-dependent anion channel 1 (VDAC1), a constituent of the mitochondrial permeability

15 The voltage-dependent anion channel 1 (VDAC1), found in the mitochondrial outer membrane, forms

16 NDUFB10), voltage-dependent anion channel 1 (VDAC1), four-and-a-half LIM domain protein 1 (FHL1) (als

17 osis, the voltage-dependent anion channel 1 (VDAC1), was linked to chemoresistance when in a truncate

18 Voltage-dependent anion channel-1 (VDAC1) is a highly regulated beta-barrel membrane protei

19 e demonstrate the involvement of VDAC1 and a VDAC1 N-terminal peptide (VDAC1-N-Ter) in Abeta cell pen

20 AC2, but not cells lacking the more abundant VDAC1, exhibited enhanced BAK oligomerization and were m

21 ers the normal interaction between Bcl-2 and VDAC1 thus reducing permeability of the outer mitochondr

22 between VDAC1 and APP, VDAC1 and Abeta, and VDAC1 and phosphorylated tau; and that reduced levels of

23 We also studied age- and VDAC1-linked, mutant APP/Abeta-induced mitochondrial dys

24 Abeta directly interacted with VDAC1 and VDAC1-N-Ter, as monitored by VDAC1 channel conductance,

25 ochondrial outer-membrane protein Bcl-xl and VDAC1.

26 abnormal interaction between VDAC1 and APP, VDAC1 and Abeta, and VDAC1 and phosphorylated tau; and t

27 her, we also studied the interaction between VDAC1 and Abeta (monomers and oligomers) and phosphoryla

28 may reduce the abnormal interaction between VDAC1 and APP, VDAC1 and Abeta, and VDAC1 and phosphoryl

29 ly found to represent the interfaces between VDAC1 monomers composing the oligomer.

30 e employed to identify contact sites between VDAC1 molecules in dimers and higher oligomers.

31 Both VDAC1 and VDAC2 are able to complement the phenotypic de

32 In conclusion, mitophagy induced by VDAC1 following SAH injury may in fact play a significan

33 g with Bcl-xL binding to the mitochondria by VDAC1-based peptides may serve to induce apoptosis in ca

34 with VDAC1 and VDAC1-N-Ter, as monitored by VDAC1 channel conductance, surface plasmon resonance, an

35 sight into the oligomeric status of cellular VDAC1 under physiological and apoptotic conditions.

36 ells expressing native VDAC1 but not certain VDAC1 mutants.

37 binds and inhibits the mitochondrial channel VDAC1.

38 ctly to the voltage-dependent anion channel (VDAC1), an integral membrane protein imbedded in the out

39 mice each harboring three distinct channels (VDAC1-3) encoded by separate genes.

40 Clinically, VDAC1-DeltaC was detected in tumor tissues of patients w

41 Hypoxic cells containing VDAC1-DeltaC were less sensitive to staurosporine- and e

42 een VDAC2 and its better-studied counterpart VDAC1.

43 f mitochondrial Ca(2+) overload via the CypD/VDAC1/Grp75/IP3R1 complex.

44 roduced at defined positions in cysteineless VDAC1 mutants, together with the use of cysteine-specifi

45 s VDAC1 and inhibits apoptosis by decreasing VDAC1-mediated Ca(2+) uptake into the mitochondria.

46 dels studied, 2 of the 15 proteins examined (VDAC1 and Pttg1) displayed robust and significant change

47 Interestingly, we found VDAC1 interacted with Abeta and phosphorylated tau in th

48 the mitochondria, where it perturbs the HK1-VDAC1 complex; increases mitochondrial permeability; and

49 Unlike the recent NMR structure of human VDAC1, the position of the voltage-sensing N-terminal se

50 cterized the binding of nucleotides to human VDAC1 (hVDAC1) on a single-residue level using NMR spect

51 Importantly, VDAC1-NP did not affect the ability of BH4-Bcl-2 to supp

52 Having identified mutations in VDAC1 that interfere with the Bcl-xL interaction, certai

53 suggested five cholesterol-binding sites in VDAC1, but direct experimental evidence for these sites

54 ion, peptides reduced [Ca(2+)]mito uptake in VDAC1 and VDAC3 knock-out but not VDAC1 and -3 double kn

55 lanar lipid bilayers, free tubulin inhibited VDAC1 and VDAC2 but not VDAC3.

56 the BH4 domain of Bcl-XL binds and inhibits VDAC1.

57 In conclusion, free tubulin inhibits VDAC1/2 and limits mitochondrial metabolism in HepG2 cel

58 rmine the relevant domain(s) of V2 involved, VDAC1 (V1) and V2 chimeric constructs were created and u

59 n channel (VDAC), comprising three isoforms--VDAC1, 2, and 3.

60 al calcium release, either by shRNA-mediated VDAC1 silencing or pharmacological inhibition, prevented

61 y involves mitochondrial and plasma membrane VDAC1, leading to mitochondrial dysfunction and apoptosi

62 In diabetic mice, VDAC1 activity was altered, resulting in a mitochondrial

63 we recently reported the isolation of mouse VDAC1 and VDAC2 cDNAs, as well as a third novel VDAC cDN

64 erol binding, we photolabeled purified mouse VDAC1 (mVDAC1) with photoactivatable cholesterol analogu

65 n VEGF signalling via the GlyT1-glycine-mTOR-VDAC1 axis pathway.

66 We engineered a double Cys mutant in murine VDAC1 that cross-links the alpha-helix to the wall of th

67 The modified murine VDAC1 exhibited typical voltage gating.

68 specific pH-dependent dimerization of murine VDAC1 (mVDAC1) identified by double electron-electron re

69 termined high-resolution structure of murine VDAC1 (mVDAC1).

70 rrel eukaryotic membrane protein, the murine VDAC1 (mVDAC1) at 2.3 A resolution, revealing a high-res

71 induced apoptosis in cells expressing native VDAC1 but not certain VDAC1 mutants.

72 uptake in VDAC1 and VDAC3 knock-out but not VDAC1 and -3 double knock-out mouse embryonic fibroblast

73 Bcl-xl, but not VDAC1, is a kinase substrate for mTOR in vitro, and mTOR

74 In the absence of VDAC1, phospho-StAR is degraded by cysteine proteases pr

75 Oligomeric assembly of VDAC1 was shown to be coupled to apoptosis induction, wi

76 dria, IkappaBalpha stabilises the complex of VDAC1 and hexokinase II (HKII), thereby preventing Bax r

77 Dissection of VDAC1 dimerization/oligomerization as presented here pro

78 er, the delivery of the N-terminal domain of VDAC1 as a synthetic peptide (VDAC1-NP) abolishes the ab

79 ents on VDAC1 and, conversely, the effect of VDAC1 on the structure of the lipid bilayer.

80 lysis demonstrated a decreased expression of VDAC1, LC3II, and an increase of ROS and Caspase-3 follo

81 mitochondria-bound hexokinase, induction of VDAC1 oligomerization, and cytochrome c release, a seque

82 her, our findings show that via induction of VDAC1-DeltaC, HIF-1 confers selective protection from ap

83 hanism of action that involves inhibition of VDAC1 oligomerization, apoptosis, and mitochondrial dysf

84 this study we demonstrate the involvement of VDAC1 and a VDAC1 N-terminal peptide (VDAC1-N-Ter) in Ab

85 imilar to miR-7 overexpression, knockdown of VDAC1 also led to a decrease in intracellular reactive o

86 jects, and significantly increased levels of VDAC1 in the cerebral cortices of 6-, 12- and 24-month-o

87 We found progressively increased levels of VDAC1 in the cortical tissues from the brains of patient

88 osphorylated tau; and that reduced levels of VDAC1, Abeta and phosphorylated tau may maintain normal

89 ervations, we propose that reduced levels of VDAC1, Abeta and phosphorylated tau may reduce the abnor

90 Notably, overexpression of VDAC1 without the 3'-UTR significantly abolished the pro

91 Reduction of VDAC1 activity with targeted gene disruption is shown to

92 through targeting 3'-untranslated region of VDAC1 mRNA.

93 lity that cholesterol-mediated regulation of VDAC1 may be facilitated through a specific binding site

94 oposide-induced cell death, and silencing of VDAC1-DeltaC or treatment with the tetracycline antibiot

95 The three-dimensional structure of VDAC1 reveals a channel formed by 19 beta-strands and an

96 The participation of the N-terminus of VDAC1 in the voltage-gating process has been well establ

97 n structural and functional understanding of VDAC1, but VDAC2 and -3 have been understudied despite h

98 uences of different membrane environments on VDAC1 and, conversely, the effect of VDAC1 on the struct

99 owever, the presence of non-cell-penetrating VDAC1-N-Ter peptide prevented Abeta cellular entry and A

100 inal domain of VDAC1 as a synthetic peptide (VDAC1-NP) abolishes the ability of BH4-Bcl-XL to suppres

101 ent of VDAC1 and a VDAC1 N-terminal peptide (VDAC1-N-Ter) in Abeta cell penetration and cell death in

102 Cepsilon can directly bind and phosphorylate VDAC1.

103 omputation-based selection of the predicated VDAC1 dimerization site, in combination with site-direct

104 hat directly interact with VDAC1 and prevent VDAC1 oligomerization, concomitant with an inhibition of

105 n voltage-dependent anion channel 1 protein (VDAC1) and amyloid beta (Abeta) and phosphorylated tau i

106 mass spectrometry, we identified 3 proteins (VDAC1, prohibitin, and mitofilin) relevant to AD that in

107 in the NCLs and has identified two proteins, VDAC1 and Pttg1, with the potential for use as in vivo b

108 ated Bcl-xL(Delta21) interacts with purified VDAC1, as revealed by microscale thermophoresis and as r

109 ximity ligation assay to detect and quantify VDAC1/IP3R1 and Grp75/IP3R1 interactions at the MAM inte

110 Abeta interacted with bilayer-reconstituted VDAC1 and increased its conductance approximately 2-fold

111 hannel conductivity of bilayer-reconstituted VDAC1.

112 L interaction, certain peptides representing VDAC1 sequences, including the N-terminal domain, were d

113 time course of minutes and does not require VDAC1 or VDAC3.

114 teins and pro-apoptotic protein such as ROS, VDAC1, LC-3II and Caspase-3.

115 Likewise, silencing VDAC1 expression by specific siRNA prevented Abeta entry

116 MAS spectra reveal a well-structured VDAC1 in 2D crystals of dimyristoylphosphatidylcholine (

117 or protein (APP) transgenic mice, we studied VDAC1 protein levels.

118 teine and catalase treatment also suppressed VDAC1-induced redistribution of Parkin.

119 romoting mitochondrial function by targeting VDAC1 expression.

120 , but not that of Bcl-2, selectively targets VDAC1 and inhibits apoptosis by decreasing VDAC1-mediate

121 We conclude that VDAC1 and CNTNAP1 associate with gamma-secretase in dete

122 These observations led us to conclude that VDAC1 interacts with Abeta, and phosphorylated tau may i

123 Recently, we demonstrated that VDAC1 oligomerization is involved in mitochondrion-media

124 To test the hypothesis that VDAC1 constitutes a pathway for ADP translocation into m

125 Moreover, the results suggest that VDAC1 also exists as a dimer that upon apoptosis inducti

126 The VDAC1 N-terminal region and two internal sequences were

127 The VDAC1-N-Ter peptide targeting Abeta cytotoxicity is thus

128 ts between the 2 organelles and involves the VDAC1/Grp75/IP3R1 complex.

129 ith a macromolecular complex composed of the VDAC1 (voltage-dependent anion channel 1), the GRP75 (ch

130 We report that CypD interacts with the VDAC1/Grp75/IP3R1 complex in cardiomyocytes.

131 and phase behavior of the lipids within the VDAC1 2D crystals.

132 mity of beta-strands 1, 2, and 19 within the VDAC1 dimer and the existence of other association sites

133 Thus, VDAC1 oligomerization represents a prime target for agen

134 promoting tumor cell survival via binding to VDAC1.

135 ociated with enhanced apoptosis and point to VDAC1 as a promising target for therapeutic intervention

136 HKII), thereby preventing Bax recruitment to VDAC1 and the release of cytochrome c for apoptosis indu

137 Direct binding of mutant SOD1 to VDAC1 inhibits conductance of individual channels when r

138 The formation of truncated VDAC1, which had a similar channel activity and voltage

139 nked to chemoresistance when in a truncated (VDAC1-DeltaC) but active form.

140 To test whether VDAC1 is required for creatine stimulation of mitochondr

141 ming that Bcl-xL interacts functionally with VDAC1 and -3 but not VDAC2.

142 evelop compounds that directly interact with VDAC1 and prevent VDAC1 oligomerization, concomitant wit

143 Bcl-xL interacted with VDAC1 and -3 isoforms, and peptides based on the VDAC se

144 Abeta directly interacted with VDAC1 and VDAC1-N-Ter, as monitored by VDAC1 channel con

145 interact with StAR before it interacts with VDAC1.

146 in beta-strands 1, 2, and 19 interfered with VDAC1 oligomerization.

147 osis, in line with the results obtained with VDAC1(-/-) cells.

148 n of the antiapoptotic protein, Bcl-xL, with VDAC1 and reveal that this interaction mediates Bcl-xL p