ライフサイエンスコーパス: VDAC

1 VDAC acts as an early sensor of lipid toxicity and its G

2 VDAC also interacts with antiapoptotic proteins from the

3 VDAC has three isoforms with >70% sequence similarity an

4 VDAC is a 283-residue integral membrane protein that for

5 VDAC is also a substrate for plasmin; hence, it mimics f

6 VDAC is characterized by its ability to "gate" between a

7 VDAC proteins function to regulate metabolites, ions, RO

8 VDAC, a major protein of the mitochondrial outer membran

9 VDACs play an important role in the regulated flux of me

10 VDACs recruit Parkin to defective mitochondria.

11 VDACs specifically interact with Parkin on defective mit

12 The voltage-dependent anion channel 1 (VDAC-1) is an important protein of the outer mitochondri

13 e kinase, voltage-dependent anion channel 1 (VDAC-1), HSP60, and Grp75.

14 involving voltage-dependent anion channel-1 (VDAC-1) and by exocytosis of ATP localized within membra

15 rs of the voltage-dependent anion channel-1 (VDAC-1) or treatment with a VDAC-1 selective blocking an

16 oltage-dependent anion channels 1, 2, and 3 (VDACs 1, 2, and 3), pore-forming proteins in the outer m

17 AC, and (ii) the ClC-2, ClC-3, ClC-4, ClC-5, VDAC, CaCC, MDR-1 and CFTR gene products do not contribu

18 between amino acids Ile(5) and Asn(37) and a VDAC region including amino acids (20)GYGFG(24).

19 itochondrial outer-membrane protein VDAC2, a VDAC isoform present in low abundance that interacts spe

20 anion channel-1 (VDAC-1) or treatment with a VDAC-1 selective blocking antibody or silencing mRNA exp

21 clear that the two nonlamellar lipids affect VDAC gating.

22 With VDAC3 to the greatest extent, all VDAC isoforms contributed to the maintenance of mitochon

23 This also amplifies VDAC enzymatic and channel activities regulation by calc

24 unocaptured not only CPT1a but also ACSL and VDAC, further strengthening findings with blue native el

25 protein interaction between CPT1a, ACSL, and VDAC.

26 sis is associated with formation of CyPD and VDAC oligomers, consistent with mPTP formation.

27 at there is an interaction between G3139 and VDAC, a protein that can facilitate the physiologic exch

28 and t-PA serve as a bridge between GRP78 and VDAC bringing them together to facilitate Pg activation.

29 and that its association with t-PA, Pg, and VDAC on the cell surface may be part of a system control

30 (PTP) to Ca2+ through a Bcl-xL-sensitive and VDAC-mediated process.

31 itochondria outer membrane protein Tom40 and VDAC are confirmed by independent mutagenesis and chemic

32 egulation of TSPO pathway proteins (TSPO and VDAC), both in terms of mRNA and protein levels.

33 optotic signaling by effecting VDAC-VDAC and VDAC-hexokinase interactions.

34 Thus, an interaction between Bcl-xL and VDAC promotes matrix Ca(2+) accumulation by increasing C

35 to the strength of participants' behavioral VDAC effect and persisted into subsequent target process

36 ffects, and their relationship to behavioral VDAC.

37 more, CHS stabilizes the interaction between VDAC and hexokinase (K(d) of 27 +/- 6 muM), confirming t

38 ysiologically detectable interaction between VDAC channels isolated from mammalian mitochondria and e

39 The functional interactions between VDAC and alpha-syn, revealed by the present study, point

40 HXK II is unable to bind VDAC phosphorylated by GSK3beta and dissociates from the

41 nuclear magnetic resonance spectra for both VDAC-1, a beta-barrel membrane protein, and the G-protei

42 Furthermore, both VDAC anion selectivity and single channel conductance in

43 ical experiments indicate that micelle-bound VDAC is in intermediate exchange between monomer and tri

44 ion of mitochondrial energetics, governed by VDAC and tubulin at the mitochondria-cytosol interface.

45 lying this value-driven attentional capture (VDAC) is that reward-associated stimulus representations

46 n termed "value-driven attentional capture" (VDAC).

47 in block of voltage-dependent anion channel (VDAC) "rescued" mitochondrial membrane potential and met

48 ch contains voltage-dependent anion channel (VDAC) 2.

49 through the voltage-dependent anion channel (VDAC) and/or adenine nucleotide transporter (ANT) or to

50 through the voltage-dependent anion channel (VDAC) because this channel provides primary permeation p

51 ane protein voltage-dependent anion channel (VDAC) blocks traffic through the channel and reduces oxi

52 The voltage-dependent anion channel (VDAC) constitutes the major pathway for the entry and ex

53 The voltage-dependent anion channel (VDAC) governs the free exchange of ions and metabolites

54 rial marker voltage-dependent anion channel (VDAC) have various expression levels in different mitoch

55 The voltage-dependent anion channel (VDAC) in the outer membrane of mitochondria serves an es

56 e-localized voltage-dependent anion channel (VDAC) is a known Ca(2+) permeability pathway that direct

57 The voltage-dependent anion channel (VDAC) is the major pathway for ATP, ADP, and other respi

58 The voltage-dependent anion channel (VDAC) is the major pathway mediating the transfer of met

59 The voltage-dependent anion channel (VDAC) is the major permeability pathway for metabolites

60 The voltage-dependent anion channel (VDAC) is the most abundant protein in the mitochondrial

61 The voltage-dependent anion channel (VDAC) is the most abundant protein in the outer mitochon

62 The voltage-dependent anion channel (VDAC) mediates and gates the flux of metabolites and ion

63 The voltage-dependent anion channel (VDAC) mediates trafficking of small molecules and ions a

64 locking the voltage-dependent anion channel (VDAC) of mitochondrial outer membrane.

65 kage of the voltage-dependent anion channel (VDAC) of the mitochondrial outer membrane by dimeric tub

66 ct with the voltage-dependent anion channel (VDAC) of the outer mitochondrial membrane.

67 entified as voltage-dependent anion channel (VDAC) oligomerization.

68 rmed by the voltage-dependent anion channel (VDAC) oligomers in the mitochondrial outer membrane.

69 Voltage-dependent anion channel (VDAC) proteins are major components of the outer mitocho

70 rylation of voltage-dependent anion channel (VDAC) through a protein kinase Cepsilon (PKCepsilon)-dep

71 al membrane voltage-dependent anion channel (VDAC) via a hydrophobic interaction that is independent

72 the murine voltage-dependent anion channel (VDAC) was determined by microcrystal electron diffractio

73 The voltage-dependent anion channel (VDAC), a major pore-forming protein in the outer membran

74 fication of voltage-dependent anion channel (VDAC), a membrane channel and NADH oxidase, as a cause o

75 ore, namely voltage-dependent anion channel (VDAC), adenine nucleotide translocase (ANT), and hexokin

76 cluding the voltage-dependent anion channel (VDAC), adenine nucleotide translocator (ANT), and cyclop

77 on with the voltage-dependent anion channel (VDAC), an abundant outer mitochondrial membrane protein.

78 e synthase, voltage-dependent anion channel (VDAC), and cytochrome c oxidase subunit 4 (COX IV).

79 through the voltage-dependent anion channel (VDAC), comprising three isoforms--VDAC1, 2, and 3.

80 rotein, the voltage-dependent anion channel (VDAC), is implicated in the control of apoptosis, includ

81 rotein, the voltage-dependent anion channel (VDAC), is increasingly implicated in the control of apop

82 (LCAS), and voltage-dependent anion channel (VDAC), isolated from rat liver mitochondrial outer membr

83 tors of the voltage-dependent anion channel (VDAC), Konig polyanion, and 4,4'-diisothiocyanatostilben

84 ed that the voltage-dependent anion channel (VDAC), located on the outer membrane of mitochondria, pl

85 tochondrial voltage-dependent anion channel (VDAC), reconstituted into planar bilayers of a plant-der

86 ties of the voltage-dependent anion channel (VDAC), the major channel in MOM.

87 dent on the voltage-dependent anion channel (VDAC), the major channel of MOM, remains controversial.

88 blocks the voltage-dependent anion channel (VDAC), the major channel of the mitochondrial outer memb

89 transporter voltage-dependent anion channel (VDAC), the protein translocator of the outer membrane 40

90 ed with the voltage-dependent anion channel (VDAC), which is also a t-PA-binding protein in these cel

91 through the voltage-dependent anion channel (VDAC)-1/glucose-regulated protein 75 (Grp75)/inositol 1,

92 he level of voltage-dependent anion channel (VDAC).

93 SL) and the voltage-dependent anion channel (VDAC).

94 ike protein voltage-dependent anion channel (VDAC).

95 and of the voltage-dependent anion channel (VDAC).

96 d the human voltage-dependent anion channel (VDAC); however, a functional relationship between these

97 f the human voltage dependent anion channel (VDAC-1) as an example of a polytopic integral membrane p

98 e voltage-dependent anion-selective channel (VDAC) and its interactions with hexokinase play integral

99 e voltage-dependent anion-selective channel (VDAC), which can form a large conductance and permanentl

100 ontent, and voltage-dependent anion channel [VDAC] content) as well as Q(10) content was determined.

101 The mitochondrial channel, VDAC, regulates metabolite flux across the outer membran

102 closure of voltage-dependent anion channels (VDAC) in the mitochondrial outer membrane after ethanol

103 The voltage-dependent anion channels (VDAC) were identified as components of M. avium vacuoles

104 Pi through voltage-dependent anion channels (VDAC).

105 Voltage-dependent anion channels (VDACs) are a family of small pore-forming proteins of th

106 mmals, the Voltage-dependent anion channels (VDACs) are predominant proteins of the outer mitochondri

107 Voltage-dependent anion channels (VDACs) are the most abundant proteins in the outer mitoc

108 y, through voltage dependant anion channels (VDACs) interacting with microtubule-associated protein 1

109 ochondrial voltage-dependent anion channels (VDACs)--a novel target for anti-cancer drugs.

110 with the titration of the negatively charged VDAC residues at low pH values.

111 ells, closing the pore and likely disrupting VDAC's flow of metabolites.

112 n the membrane, whereas cardiolipin disrupts VDAC supramolecular assemblies.

113 Each VDAC is sufficient to support Parkin recruitment and mit

114 dulation of apoptotic signaling by effecting VDAC-VDAC and VDAC-hexokinase interactions.

115 -dependent rate at which a membrane-embedded VDAC nanopore captures alpha-syn is a strong function of

116 ed VDAC-1 resemble those of micelle-embedded VDAC-1, indicating a similar structure and function in t

117 the native ligand NADH to nanodisc-embedded VDAC-1 resemble those of micelle-embedded VDAC-1, indica

118 Four nucleus-encoded VDACs have been identified in Arabidopsis thaliana.

119 e demonstrate that PG significantly enhances VDAC oligomerization in the membrane, whereas cardiolipi

120 owever, it still remains unknown how exactly VDAC supramolecular assembly can be regulated in the mem

121 ogaster, porin is the ubiquitously expressed VDAC isoform.

122 NMR spectroscopy demonstrates a well folded VDAC-1 protein and native NADH binding functionality.

123 the theory with experiments is excellent for VDAC.

124 ese results demonstrate a novel function for VDAC-1 as the conductive mechanism responsible for Alter

125 nt and validation of a new in vivo model for VDAC function in Drosophila should provide a valuable to

126 ipulations proved GSK3 to be responsible for VDAC phosphorylation in normal cells.

127 These results establish a novel role for VDAC-1 as a mechanism underlying ATP release induced by

128 at much higher voltages than is typical for VDAC.

129 f mitochondrial porins that is distinct from VDAC, TOM40, and MDM10.

130 Here, VDAC has been expressed, purified, and refolded into a f

131 ve oxygen consumption ratio (OCR) and higher VDAC protein levels when compared to WT and Myd88(-/-) c

132 These results highlight VDAC-2 as a critical inhibitor of Bak-mediated apoptotic

133 xplore the ion transport properties of human VDAC isoform 1 (hVDAC1; PDB:2K4T) embedded in an implici

134 mus molecular dynamics simulations of human VDAC isoform 1 in DOPE/DOPC mixed bilayers in 1 M KCl so

135 NMR) solution structure of recombinant human VDAC-1 reconstituted in detergent micelles.

136 We find that PE induces voltage asymmetry in VDAC current-voltage characteristics by promoting channe

137 of tubulin result in substantial changes in VDAC closure.

138 The observed differences in VDAC behavior in PC and PE membranes cannot be explained

139 results, and the known importance of E73 in VDAC physiology, VDAC dimerization likely plays a signif

140 that PKA and GSK-3beta decrease and increase VDAC conductance, respectively.

141 Tubulin strikingly increases VDAC voltage sensitivity and at physiological salt condi

142 t physiological salt conditions could induce VDAC closure at <10 mV transmembrane potentials.

143 intact cells and antagonized tubulin-induced VDAC blockage in planar bilayers.

144 Thus, inhibiting VDAC oligomerization is a potential therapeutic approach

145 icate at least a partial entry of G3139 into VDAC, forming an unstable bound state, which is responsi

146 een R6/2 and WT included: in striatum, lower VDAC and the mitochondrially encoded cytochrome oxidase

147 Next, we measured VDAC in a separate task by presenting these stimuli in t

148 on channel from outer mitochondrial membrane VDAC, bacterial porin OmpC (outer membrane protein C), a

149 the L-type Ca(2+) channel and mitochondrial VDAC.

150 The mitochondrial VDAC coimmunoprecipitated with the L-type Ca(2+) channel

151 polarity, and membrane composition modulate VDAC currents.

152 l phenotypes remarkably reminiscent of mouse VDAC mutants.

153 Notably, VDAC phosphorylation level correlated with steatosis sev

154 for the NADH-dependent reductase activity of VDAC.

155 Various small to large assemblies of VDAC are observed in mitochondrial outer membranes, but

156 ilized cells, suggesting low availability of VDAC pores within the cell.

157 ydeoxythymidine, induces partial blockage of VDAC and a change in selectivity from favoring anions to

158 that prior to the characteristic blockage of VDAC, tubulin first binds to the membrane in a lipid-dep

159 se it has been suggested that the closure of VDAC leads to the opening of another outer mitochondrial

160 duce voltage-sensitive reversible closure of VDAC reconstituted into planar phospholipid membranes.

161 s tubulin promotes single-channel closure of VDAC, we hypothesized that tubulin is a dynamic regulato

162 enesis in hepatocytes mediated by closure of VDAC.

163 TP is a heterooligomeric complex composed of VDAC, SPG7, and CypD.

164 early indicate a fundamental conservation of VDAC function.

165 ata showed that 1), the physical diameter of VDAC pores in cardiac mitochondria is >or=3 nm but <or=6

166 uable tool for further genetic dissection of VDAC role(s) in mitochondrial biology and disease, and a

167 ce from the electrophysiologic evaluation of VDAC channels reconstituted into phospholipid membranes

168 imulations and single-channel experiments of VDAC-1 show agreement for the current-voltage relationsh

169 IL-33 release by lowering the expression of VDAC-1 in the plasma membrane.

170 Electron microscopy reveals the formation of VDAC-1 multimers, an observation that is consistent with

171 The essential life-sustaining function of VDAC in metabolite trafficking is believed to be regulat

172 ith caspase-8 affected the voltage gating of VDAC by inducing channel closure.

173 The inactivation of VDAC-1 function either by pharmacological means or siRNA

174 nin-permeabilized hepatocytes, indicative of VDAC closure.

175 We propose that inhibition of VDAC by free tubulin limits mitochondrial metabolism in

176 Inhibition of VDAC-1 blocked Alternaria-evoked Ca(2+) uptake across th

177 Moreover, inhibition of VDAC-1 channel activity or reducing protein expression b

178 this is due to the preferential insertion of VDAC into CL-rich domains.

179 The involvement of VDAC oligomerization in apoptosis has been suggested in

180 Although multiple isoforms of VDAC have been found in different organisms, only one is

181 etailed analysis of the blockage kinetics of VDAC reconstituted into planar lipid membranes suggests

182 lipid accumulation triggers a rapid lack of VDAC phosphorylation by glycogen synthase kinase 3 (GSK3

183 d IL-33 secretion by decreasing the level of VDAC-1 expression in the plasma membrane.

184 Here, we show that the mechanism of VDAC blockage by tubulin involves tubulin interaction wi

185 Microcrystals of an essential mutant of VDAC grew in a viscous bicelle suspension, making it uns

186 way via the induction and oligomerization of VDAC.

187 differences in the insertion orientation of VDAC in these membranes.

188 al alpha-helix is located inside the pore of VDAC in the open state and remains associated with beta-

189 nhibited by NADH and require the presence of VDAC, a voltage-dependent anion channel present in the o

190 culate that by decreasing the probability of VDAC opening, Bid reduces metabolite exchange between mi

191 Here, we report that properties of VDAC channels reconstituted into planar phospholipid mem

192 The off-rate of VDAC blockage by tubulin does not depend on the lipid co

193 hermore, the simvastatin-evoked reduction of VDAC-1 expression in the plasma membrane, suggests the p

194 ity of TbTim50 plays a role in regulation of VDAC expression.

195 We also found that the response of VDAC gating to acidification was highly asymmetric.

196 Although, we could not establish a role of VDAC channels in the transport of known secreted M. aviu

197 helpful insights into the regulatory role of VDAC in the protective effect of cytosolic acidification

198 difference leads to the anion selectivity of VDAC.

199 The similarity of VDAC mutant phenotypes in the fly and mouse clearly indi

200 R measurements revealed the binding sites of VDAC-1 for the Bcl-2 protein Bcl-x(L), for reduced beta-

201 The tubulin-blocked state of VDAC is impermeant for ATP but only partially closed for

202 l cue for regulating the oligomeric state of VDAC.

203 The various oligomeric states of VDAC induced by the addition of CHS were deciphered thro

204 The available structures of VDAC proteins show a wide beta-stranded barrel pore, wit

205 ions contribute to differential stability of VDACs and may have implications in their in vivo regulat

206 However, the oligomeric VDAC-2 complexes are diminished, and Bak does not intera

207 not induce cytochrome c release by acting on VDAC.

208 or mitochondria metabolism and apoptosis, on VDAC oligomerization.

209 nd [K+], we determined the effect of Ca2+ on VDAC activity.

210 that alpha-syn toxicity in yeast depends on VDAC.

211 other ansamycins are due to their effects on VDAC and that this may play a role in their clinical act

212 Here, we study the effects of temperature on VDAC channels reconstituted in planar lipid membranes at

213 investigated the effects of pH variations on VDAC gating properties.

214 unctionally demarcate hVDAC-2 from the other VDACs.

215 The maxi Cl- channel (p-VDAC) blocker Gd3+, the ClC-2 inhibitor Cd2+, and the MD

216 kt, GSK3beta is activated and phosphorylates VDAC.

217 known importance of E73 in VDAC physiology, VDAC dimerization likely plays a significant role in mit

218 bition of binding and even induces prolonged VDAC closures.

219 y undescribed mutant of the membrane protein VDAC, crystallized in a lipid bicelle matrix and solved

220 283-residue integral human membrane protein VDAC-1, which has a rotational correlation time of about

221 mediated by binding to an accessory protein, VDAC-1.

222 In liposomes, the purified VDAC displays Ca2+-dependent control of the molecular cu

223 ments, at submicromolar [Ca2+], the purified VDAC or isolated OMM does not show sustained large condu

224 In the presence of cholesterol, recombinant VDAC-1 can form voltage-gated channels in phospholipid b

225 We reconstituted VDAC into planar lipid membranes and found that acidific

226 into mitochondria and significantly reduced VDAC oligomerization and AIF release.

227 he mechanisms for how these factors regulate VDAC-1, and which changes they trigger in the channel, a

228 de transport data suggest that GSK regulates VDAC and that VDAC may be an important regulatory site i

229 r, our data indicate that mitoNEET regulates VDAC in a redox-dependent manner in cells, closing the p

230 ght influence MOM permeability by regulating VDAC gating.

231 ng purified mitochondria expressing a single VDAC isoform, we found that erastin alters the permeabil

232 do not predominate in detergent-solubilized VDAC samples.

233 to induce the formation of detergent-soluble VDAC multimers.

234 -oligomeric complexes that still retain some VDAC-2.

235 Thus, in nonalcoholic steatosis VDAC exhibits reduced threonine phosphorylation, which i

236 The submicrosecond VDAC-1 voltage response shows intrinsic structural chang

237 There is accumulating evidence supporting VDAC's role in mitochondrial metabolic regulation and ap

238 Cell surface VDAC is a receptor for plasminogen kringle 5, which prom

239 re consistent with pore blockage rather than VDAC closure.

240 ata suggest that GSK regulates VDAC and that VDAC may be an important regulatory site in ischemia/rep

241 , thus initiating apoptosis, it appears that VDAC may be an important pharmacologic target of G3139.

242 In this study, we demonstrate that VDAC binds tissue-type plasminogen activator (t-PA) on h

243 ool to probe bilayer mechanics, we show that VDAC channels are much more sensitive to the presence of

244 We further suggest that VDAC can occur in the absence of changes in early visual

245 Our results suggest that VDAC is underpinned by learned value signals that modula

246 We hypothesize that VDACs serve as mitochondrial docking sites to recruit Pa

247 n recruitment and mitophagy, suggesting that VDACs can function redundantly.

248 The VDAC oligomerization inhibitor VBIT-4 decreases mtDNA re

249 The VDAC-interacting region of Bcl-xL was characterized by N

250 tubulin's negatively charged tail enters the VDAC pore, inverting its anionic selectivity to cationic

251 However, the VDAC level was unaltered when the phosphatase-inactive m

252 e occurs preferentially from one side of the VDAC channel.

253 omolar G3139 induces rapid flickering of the VDAC conductance and, occasionally, a complete conductan

254 Addition of the VDAC inhibitor 4,4'-diisothiocyanatostilbene-2,2'-disulf

255 tage-dependent asymmetric distortions of the VDAC-1 barrel and the displacement of particular charged

256 onductance, indicating a closed state of the VDAC.

257 Our characterization of the VDAC/Bcl-xL complex offers initial structural insight in

258 1 and -3 isoforms, and peptides based on the VDAC sequence disrupted Bcl-xL binding.

259 otes or ergosterol in fungi may regulate the VDAC oligomeric state and may provide a potential target

260 ce of intracellular barriers restricting the VDAC pore availability in vivo.

261 eir temperature dependence suggests that the VDAC structure does not change conformation above and be

262 of ions and metabolites passing through the VDAC pore.

263 itochondrial intermembrane space through the VDAC.

264 Thus, the VDAC gating is dependent on the physiological concentrat

265 Bcl-x(L) interacts with the VDAC barrel laterally at strands 17 and 18.

266 These VDAC residues correspond to a GXXXG repeat motif commonl

267 In the absence of all three VDACs, the recruitment of Parkin to defective mitochondr

268 ve effects of HKI and HKII, possibly through VDAC phosphorylation by PKCepsilon.

269 ious proposal that ATP translocation through VDAC is facilitated by a set of specific interactions be

270 The titration method is then applied to VDAC, a 19-stranded beta-barrel with 283 residues, for w

271 . avium mmpL4 proteins were found to bind to VDAC-1 protein.

272 and beta-tubulin tails contribute equally to VDAC blockade and what effects might be due to sequence

273 These results demonstrate that ligands to VDAC proteins can induce non-apoptotic cell death select

274 Binding of t-PA to VDAC induced a decrease in K(m) and an increase in the V

275 Binding of t-PA to VDAC occurs between a t-PA fibronectin type I finger dom

276 uorescence cross-correlation spectroscopy to VDAC reconstituted into giant unilamellar vesicles, we d

277 referentially localized in close vicinity to VDAC, presumably at the inner boundary membrane, whereas

278 ned direct evidence for binding of Bcl-xL to VDAC in a detergent micelle system.

279 The data reported here suggest that TSPO-VDAC complex upregulation in BD patients, the simultaneo

280 Reversal of tubulin-VDAC interaction by erastin antagonizes Warburg metaboli

281 find that voltage sensitivity of the tubulin-VDAC blockage practically does not depend on the lipid c

282 This tubulin-VDAC interaction requires tubulin anionic C-terminal tai

283 nce mitochondrial respiration through tuning VDAC sensitivity to blockage by tubulin.

284 s suggest that Bcl-xL can bind to one or two VDAC molecules forming heterodimers and heterotrimers.

285 resistance to erastin, implicating these two VDAC isoforms in the mechanism of action of erastin.

286 The neural mechanisms underlying VDAC remain unclear.

287 s resulted in accelerated Pg activation when VDAC, t-PA, and Pg were bound together.

288 These phenomena occur only when VDAC is in the "open" conformation and therefore are con

289 al metabolic regulation and apoptosis, where VDAC oligomerization has been implicated with these proc

290 hagy-related proteins and TSPO levels, while VDAC correlated negatively with p62/SQSTM1 and LC3 prote

291 nstrated the direct interaction of Bcl2 with VDAC, leading to reduced channel conductance.

292 rtical areas, an effect that correlates with VDAC, we find no relevant signatures of changes in early

293 Experiments with VDAC-1 mutants identified amino acids that regulate the

294 e diminished, and Bak does not interact with VDAC-2 in Bax-deficient HCT116 cells.

295 rrelated with their ability to interact with VDAC.

296 , perhaps partly via direct interaction with VDAC and reduction of metabolite flow across the mitocho

297 c Bcl-xL may be through its interaction with VDAC.

298 Erastin, a compound that interacts with VDAC, blocked and reversed mitochondrial depolarization

299 ntibodies against these sequences react with VDAC and detect this protein on the plasma membrane of h

300 rate that Parkin specifically interacts with VDACs when the function of mitochondria is disrupted by