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1                                              VDAC1 and phosphate carrier protein are the first OMM pr
2                                              VDAC1 co-purifies with cholesterol and is functionally r
3                                              VDAC1 inhibition perturbed pyruvate metabolism, elicitin
4                                              VDAC1 is a crucial player in the cross talk between the
5                                              VDAC1 is overexpressed in post-mortem brains of Alzheime
6                                              VDAC1 KO specifically reduced glycolytic activity linked
7                                              VDAC1, ANT1, and HKII were present in the PKCepsilon com
8                                              VDAC1, which controls metabolism, lipids transport, apop
9                                              VDAC1-based peptides interacted with Bcl2 to prevent its
10                                              VDAC1-DeltaC may also hold promise as a biomarker for tu
11 leased by voltage-dependent anion channel 1 (VDAC1) after sciatic nerve injury triggers Schwann cell
12 articular voltage-dependent anion channel 1 (VDAC1) and contactin-associated protein 1 (CNTNAP1), red
13 ) and the voltage-dependent anion channel 1 (VDAC1) at the outer mitochondrial membranes.
14 Voltage-dependent anion-selective channel 1 (VDAC1) in DECs.
15 ession of voltage-dependent anion channel 1 (VDAC1) induced Parkin translocation to mitochondria, pre
16 e protein voltage-dependent anion channel 1 (VDAC1) is a convergence point for a variety of cell surv
17 ounded to voltage dependent anion channel 1 (VDAC1) on the mitochondrial outer membrane and inhibited
18 acts with voltage-dependent anion channel 1 (VDAC1) on the OMM, which then facilitates processing of
19 ession of voltage-dependent anion channel 1 (VDAC1), a constituent of the mitochondrial permeability
20 ndria via voltage-dependent anion channel 1 (VDAC1), are abundant in Tregs.
21       The voltage-dependent anion channel 1 (VDAC1), found in the mitochondrial outer membrane, forms
22 NDUFB10), voltage-dependent anion channel 1 (VDAC1), four-and-a-half LIM domain protein 1 (FHL1) (als
23 tein, the voltage-dependent-anion channel 1 (VDAC1), in gastrointestinal inflammation and tested the
24 osis, the voltage-dependent anion channel 1 (VDAC1), was linked to chemoresistance when in a truncate
25 ) protein voltage-dependent anion channel 1 (VDAC1).
26  with the voltage-dependent anion channel-1 (VDAC1) in mitochondria and that INSR knockdown triggers
27           Voltage-dependent anion channel-1 (VDAC1) is a highly regulated beta-barrel membrane protei
28 1 and the voltage-dependent anion channel-1 (VDAC1), interfering with their association.
29 dependent anion-selective channel protein 1 (VDAC1) and N-methyl-D-aspartate receptor 1 (NMDAR1) were
30 e demonstrate the involvement of VDAC1 and a VDAC1 N-terminal peptide (VDAC1-N-Ter) in Abeta cell pen
31 ronal mitochondrial DNA (mtDNA) efflux via a VDAC1-dependent mechanism, activating the innate immune
32 AC2, but not cells lacking the more abundant VDAC1, exhibited enhanced BAK oligomerization and were m
33 ers the normal interaction between Bcl-2 and VDAC1 thus reducing permeability of the outer mitochondr
34  between VDAC1 and APP, VDAC1 and Abeta, and VDAC1 and phosphorylated tau; and that reduced levels of
35                     We also studied age- and VDAC1-linked, mutant APP/Abeta-induced mitochondrial dys
36 sensitive regulation of the ATP synthase and VDAC1, the channel that releases ATP into the cytosol.
37 ed oxidative phosphorylation complex I-V and VDAC1 abundance partially explain decreased skeletal mus
38     Abeta directly interacted with VDAC1 and VDAC1-N-Ter, as monitored by VDAC1 channel conductance,
39 ochondrial outer-membrane protein Bcl-xl and VDAC1.
40  abnormal interaction between VDAC1 and APP, VDAC1 and Abeta, and VDAC1 and phosphorylated tau; and t
41 her, we also studied the interaction between VDAC1 and Abeta (monomers and oligomers) and phosphoryla
42  may reduce the abnormal interaction between VDAC1 and APP, VDAC1 and Abeta, and VDAC1 and phosphoryl
43 also demonstrate unique interactions between VDAC1 and other receptor tyrosine kinases, indicating a
44 ly found to represent the interfaces between VDAC1 monomers composing the oligomer.
45 e employed to identify contact sites between VDAC1 molecules in dimers and higher oligomers.
46                                         Both VDAC1 and VDAC2 are able to complement the phenotypic de
47          In conclusion, mitophagy induced by VDAC1 following SAH injury may in fact play a significan
48 g with Bcl-xL binding to the mitochondria by VDAC1-based peptides may serve to induce apoptosis in ca
49  with VDAC1 and VDAC1-N-Ter, as monitored by VDAC1 channel conductance, surface plasmon resonance, an
50       We conclude that UC may be promoted by VDAC1-overexpression and may therefore be amenable to tr
51  are three VDAC isoforms in mammalian cells, VDAC1, VDAC2, and VDAC3, with varying tissue-specific ex
52 sight into the oligomeric status of cellular VDAC1 under physiological and apoptotic conditions.
53 ells expressing native VDAC1 but not certain VDAC1 mutants.
54 binds and inhibits the mitochondrial channel VDAC1.
55 d MFF2) and voltage-dependent anion channel (VDAC1) as a novel regulator of mitochondrial cell death
56 A5 with the voltage-dependent anion channel (VDAC1) in the outer mitochondrial membrane (OMM).
57 ctly to the voltage-dependent anion channel (VDAC1), an integral membrane protein imbedded in the out
58 dentify the voltage-dependent anion channels VDAC1 and VDAC2 as mitochondrial ceramide binding protei
59 mice each harboring three distinct channels (VDAC1-3) encoded by separate genes.
60                                  Clinically, VDAC1-DeltaC was detected in tumor tissues of patients w
61                     Hypoxic cells containing VDAC1-DeltaC were less sensitive to staurosporine- and e
62                  Furthermore, by controlling VDAC1's oligomeric state, AnxA5 is protective against ci
63 een VDAC2 and its better-studied counterpart VDAC1.
64 f mitochondrial Ca(2+) overload via the CypD/VDAC1/Grp75/IP3R1 complex.
65 roduced at defined positions in cysteineless VDAC1 mutants, together with the use of cysteine-specifi
66 s VDAC1 and inhibits apoptosis by decreasing VDAC1-mediated Ca(2+) uptake into the mitochondria.
67 nd tested the effects of the newly developed VDAC1-interacting molecules, VBIT-4 and VBIT-12, on UC i
68 limit of cryo-electron microscopy (cryo-EM), VDAC1's 31 kDa size has long been a bottleneck in determ
69 dels studied, 2 of the 15 proteins examined (VDAC1 and Pttg1) displayed robust and significant change
70 sated for by the more ubiquitously expressed VDAC1 and VDAC2 isoforms.
71                      Interestingly, we found VDAC1 interacted with Abeta and phosphorylated tau in th
72 sical properties that distinguish VDAC2 from VDAC1 and VDAC3.
73 tive [2Fe-2S] cluster protein mitoNEET gates VDAC1 when mitoNEET is oxidized.
74  the mitochondria, where it perturbs the HK1-VDAC1 complex; increases mitochondrial permeability; and
75 tion into membrane vesicles, dimers of human VDAC1 and VDAC2 catalyze rapid transbilayer translocatio
76 dimensional (2D) crystalline sample of human VDAC1 in lipids, we applied proton-detected fast magic-a
77     Unlike the recent NMR structure of human VDAC1, the position of the voltage-sensing N-terminal se
78 cterized the binding of nucleotides to human VDAC1 (hVDAC1) on a single-residue level using NMR spect
79 ta and innate immune activation, identifying VDAC1, the AGE-RAGE axis, and the cGAS-STING pathway as
80                                 Importantly, VDAC1-NP did not affect the ability of BH4-Bcl-2 to supp
81               Having identified mutations in VDAC1 that interfere with the Bcl-xL interaction, certai
82  suggested five cholesterol-binding sites in VDAC1, but direct experimental evidence for these sites
83 ion, peptides reduced [Ca(2+)]mito uptake in VDAC1 and VDAC3 knock-out but not VDAC1 and -3 double kn
84 ltured colon cells inhibited the DSS-induced VDAC1 overexpression, oligomerization, and apoptosis.
85 lanar lipid bilayers, free tubulin inhibited VDAC1 and VDAC2 but not VDAC3.
86  the BH4 domain of Bcl-XL binds and inhibits VDAC1.
87         In conclusion, free tubulin inhibits VDAC1/2 and limits mitochondrial metabolism in HepG2 cel
88 rmine the relevant domain(s) of V2 involved, VDAC1 (V1) and V2 chimeric constructs were created and u
89 n channel (VDAC), comprising three isoforms--VDAC1, 2, and 3.
90     Using alpha-synuclein (alphaSyn)-a known VDAC1 cytosolic regulator-we found that higher-conductan
91 al calcium release, either by shRNA-mediated VDAC1 silencing or pharmacological inhibition, prevented
92 y involves mitochondrial and plasma membrane VDAC1, leading to mitochondrial dysfunction and apoptosi
93                            In diabetic mice, VDAC1 activity was altered, resulting in a mitochondrial
94  we recently reported the isolation of mouse VDAC1 and VDAC2 cDNAs, as well as a third novel VDAC cDN
95 erol binding, we photolabeled purified mouse VDAC1 (mVDAC1) with photoactivatable cholesterol analogu
96 n VEGF signalling via the GlyT1-glycine-mTOR-VDAC1 axis pathway.
97  We engineered a double Cys mutant in murine VDAC1 that cross-links the alpha-helix to the wall of th
98                          The modified murine VDAC1 exhibited typical voltage gating.
99 specific pH-dependent dimerization of murine VDAC1 (mVDAC1) identified by double electron-electron re
100 termined high-resolution structure of murine VDAC1 (mVDAC1).
101 rrel eukaryotic membrane protein, the murine VDAC1 (mVDAC1) at 2.3 A resolution, revealing a high-res
102 induced apoptosis in cells expressing native VDAC1 but not certain VDAC1 mutants.
103  uptake in VDAC1 and VDAC3 knock-out but not VDAC1 and -3 double knock-out mouse embryonic fibroblast
104                              Bcl-xl, but not VDAC1, is a kinase substrate for mTOR in vitro, and mTOR
105 herefore be amenable to treatment with novel VDAC1-interacting molecules.
106                            In the absence of VDAC1, phospho-StAR is degraded by cysteine proteases pr
107                       Oligomeric assembly of VDAC1 was shown to be coupled to apoptosis induction, wi
108 dria, IkappaBalpha stabilises the complex of VDAC1 and hexokinase II (HKII), thereby preventing Bax r
109                               The content of VDAC1 and IP3R, proteins involved in ER-mitochondria com
110                        This disengagement of VDAC1 from hexokinase-1 resulted in activation of apopto
111                                Dissection of VDAC1 dimerization/oligomerization as presented here pro
112 er, the delivery of the N-terminal domain of VDAC1 as a synthetic peptide (VDAC1-NP) abolishes the ab
113 charged residues in the N-terminal domain of VDAC1 interact with mtDNA, promoting VDAC1 oligomerizati
114 ents on VDAC1 and, conversely, the effect of VDAC1 on the structure of the lipid bilayer.
115 lysis demonstrated a decreased expression of VDAC1, LC3II, and an increase of ROS and Caspase-3 follo
116  mitochondria-bound hexokinase, induction of VDAC1 oligomerization, and cytochrome c release, a seque
117 her, our findings show that via induction of VDAC1-DeltaC, HIF-1 confers selective protection from ap
118 hanism of action that involves inhibition of VDAC1 oligomerization, apoptosis, and mitochondrial dysf
119 NG, as well as pharmacological inhibition of VDAC1, protected APP mice from mitochondrial dysfunction
120 this study we demonstrate the involvement of VDAC1 and a VDAC1 N-terminal peptide (VDAC1-N-Ter) in Ab
121 imilar to miR-7 overexpression, knockdown of VDAC1 also led to a decrease in intracellular reactive o
122 jects, and significantly increased levels of VDAC1 in the cerebral cortices of 6-, 12- and 24-month-o
123   We found progressively increased levels of VDAC1 in the cortical tissues from the brains of patient
124 osphorylated tau; and that reduced levels of VDAC1, Abeta and phosphorylated tau may maintain normal
125 ervations, we propose that reduced levels of VDAC1, Abeta and phosphorylated tau may reduce the abnor
126                   Notably, overexpression of VDAC1 without the 3'-UTR significantly abolished the pro
127                                 Reduction of VDAC1 activity with targeted gene disruption is shown to
128  through targeting 3'-untranslated region of VDAC1 mRNA.
129 lity that cholesterol-mediated regulation of VDAC1 may be facilitated through a specific binding site
130 y uncovers AnxA5 as an integral regulator of VDAC1 in physiological and pathological conditions.
131 ase 3 beta, a putative negative regulator of VDAC1, and a hypermetabolic state that amplified Treg in
132 oposide-induced cell death, and silencing of VDAC1-DeltaC or treatment with the tetracycline antibiot
133 se-grained molecular dynamics simulations of VDAC1 reveal that lipid scrambling occurs at a specific
134 M by promoting the Ca(2+)-permeable state of VDAC1.
135           The three-dimensional structure of VDAC1 reveals a channel formed by 19 beta-strands and an
136       The participation of the N-terminus of VDAC1 in the voltage-gating process has been well establ
137 n structural and functional understanding of VDAC1, but VDAC2 and -3 have been understudied despite h
138 uences of different membrane environments on VDAC1 and, conversely, the effect of VDAC1 on the struct
139 owever, the presence of non-cell-penetrating VDAC1-N-Ter peptide prevented Abeta cellular entry and A
140 inal domain of VDAC1 as a synthetic peptide (VDAC1-NP) abolishes the ability of BH4-Bcl-XL to suppres
141 ent of VDAC1 and a VDAC1 N-terminal peptide (VDAC1-N-Ter) in Abeta cell penetration and cell death in
142 Cepsilon can directly bind and phosphorylate VDAC1.
143 omputation-based selection of the predicated VDAC1 dimerization site, in combination with site-direct
144 hat directly interact with VDAC1 and prevent VDAC1 oligomerization, concomitant with an inhibition of
145 main of VDAC1 interact with mtDNA, promoting VDAC1 oligomerization.
146 n voltage-dependent anion channel 1 protein (VDAC1) and amyloid beta (Abeta) and phosphorylated tau i
147 mass spectrometry, we identified 3 proteins (VDAC1, prohibitin, and mitofilin) relevant to AD that in
148 in the NCLs and has identified two proteins, VDAC1 and Pttg1, with the potential for use as in vivo b
149 ated Bcl-xL(Delta21) interacts with purified VDAC1, as revealed by microscale thermophoresis and as r
150 ximity ligation assay to detect and quantify VDAC1/IP3R1 and Grp75/IP3R1 interactions at the MAM inte
151  Abeta interacted with bilayer-reconstituted VDAC1 and increased its conductance approximately 2-fold
152 hannel conductivity of bilayer-reconstituted VDAC1.
153 L interaction, certain peptides representing VDAC1 sequences, including the N-terminal domain, were d
154  time course of minutes and does not require VDAC1 or VDAC3.
155 teins and pro-apoptotic protein such as ROS, VDAC1, LC-3II and Caspase-3.
156                          Likewise, silencing VDAC1 expression by specific siRNA prevented Abeta entry
157         MAS spectra reveal a well-structured VDAC1 in 2D crystals of dimyristoylphosphatidylcholine (
158 or protein (APP) transgenic mice, we studied VDAC1 protein levels.
159 teine and catalase treatment also suppressed VDAC1-induced redistribution of Parkin.
160 romoting mitochondrial function by targeting VDAC1 expression.
161 , but not that of Bcl-2, selectively targets VDAC1 and inhibits apoptosis by decreasing VDAC1-mediate
162                             We conclude that VDAC1 and CNTNAP1 associate with gamma-secretase in dete
163   These observations led us to conclude that VDAC1 interacts with Abeta, and phosphorylated tau may i
164               Recently, we demonstrated that VDAC1 oligomerization is involved in mitochondrion-media
165                  To test the hypothesis that VDAC1 constitutes a pathway for ADP translocation into m
166           Moreover, the results suggest that VDAC1 also exists as a dimer that upon apoptosis inducti
167                                          The VDAC1 N-terminal region and two internal sequences were
168                                          The VDAC1-N-Ter peptide targeting Abeta cytotoxicity is thus
169 ts between the 2 organelles and involves the VDAC1/Grp75/IP3R1 complex.
170 ith a macromolecular complex composed of the VDAC1 (voltage-dependent anion channel 1), the GRP75 (ch
171       We report that CypD interacts with the VDAC1/Grp75/IP3R1 complex in cardiomyocytes.
172  and phase behavior of the lipids within the VDAC1 2D crystals.
173 mity of beta-strands 1, 2, and 19 within the VDAC1 dimer and the existence of other association sites
174                                         This VDAC1-based strategy exploits a completely new target fo
175                                        Thus, VDAC1 oligomerization represents a prime target for agen
176 promoting tumor cell survival via binding to VDAC1.
177 ociated with enhanced apoptosis and point to VDAC1 as a promising target for therapeutic intervention
178 HKII), thereby preventing Bax recruitment to VDAC1 and the release of cytochrome c for apoptosis indu
179             Direct binding of mutant SOD1 to VDAC1 inhibits conductance of individual channels when r
180                   The formation of truncated VDAC1, which had a similar channel activity and voltage
181 nked to chemoresistance when in a truncated (VDAC1-DeltaC) but active form.
182                                       Unlike VDAC1 removal, loss of VDAC2 or replacing its membrane-f
183                              To test whether VDAC1 is required for creatine stimulation of mitochondr
184 ming that Bcl-xL interacts functionally with VDAC1 and -3 but not VDAC2.
185 evelop compounds that directly interact with VDAC1 and prevent VDAC1 oligomerization, concomitant wit
186                       Bcl-xL interacted with VDAC1 and -3 isoforms, and peptides based on the VDAC se
187               Abeta directly interacted with VDAC1 and VDAC1-N-Ter, as monitored by VDAC1 channel con
188 se data demonstrate that INSR interacts with VDAC1 to mediate mitochondrial stability.
189  interact with StAR before it interacts with VDAC1.
190 in beta-strands 1, 2, and 19 interfered with VDAC1 oligomerization.
191 osis, in line with the results obtained with VDAC1(-/-) cells.
192 n of the antiapoptotic protein, Bcl-xL, with VDAC1 and reveal that this interaction mediates Bcl-xL p

 
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