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VDAC1 allows Ca(2+) access to the MCU, facilitating transport of Ca(2+) to the matrix, and also from the IMS to the cytosol. Intra-mitochondrial Ca(2+) controls energy production and metabolism by modulating critical enzymes in the tricarboxylic acid (TCA) cycle and fatty acid oxidation.
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associate dysfunction in Fe-S cluster biogenesis with cleavage of VDAC1
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HK1 competes with SOD1 G93A mutant from familial amyotrophic lateral sclerosis cases for binding VDAC1.SOD1 G93A mutant from familial amyotrophic lateral sclerosis cases binds VDAC1 with high affinity.
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Study shows that silencing voltage-dependent anion channel 1 (VDAC1) expression using short interfering RNA-VDAC1 in 9 glioblastoma-related cell lines, including patient-derived cells, led to marked decreases in VDAC1 levels and cell growth.
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VDAC1 plays an important role in dengue virus infection.
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VDAC1 is a direct target of miR-320a in non-small cell lung cancer (NSCLC) cells, and miR-320a inhibits VDAC1 expression in NSCLC cells
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The results of this study shown VDAC1, the Potential Target of miR-320a, is Upregulated in Response to HIV-1 Tat.
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the present study indicated that VDAC1 may interact with HPV16 E7 to promote the malignant progression of HPV-related cervical cancer
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Porin expression was lower in patients with heart failure with preserved ejection fraction compared to controls.
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Studied voltage-dependent anion channel 1 (VDAC1) structure and oligomerization using an Escherichia coli cell-free protein synthesis system and bicelle crystallization.
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In this study, molecular dynamics simulations and single-channel experiments of VDAC-1 show agreement for the current-voltage relationships of an "open" channel and they also show several subconducting transient states that are more cation selective in the simulations. We observed voltage-dependent asymmetric distortions of the VDAC-1 barrel and the displacement of particular charged amino acids.
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VDAC1 was accumulated in the desmin highly stained area of muscle fibers of desminopathy patients.
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work raises the interesting possibility that cholesterol-mediated regulation of VDAC1 may be facilitated through a specific binding site at the functionally important Glu(73) residue.
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this study describes novel drug candidates with a defined mechanism of action that involves inhibition of VDAC1 oligomerization, apoptosis, and mitochondrial dysfunction. The compounds VBIT-3 and VBIT-4 offer a therapeutic strategy for treating different diseases associated with enhanced apoptosis and point to VDAC1 as a promising target for therapeutic intervention.
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Results from the simulations show that HK2 binding restricts the movement of the VDAC1 N-terminal helix. As a result, VDAC1 is kept in the open state most of the time and probably allows a constant supply of ATP to HK2 for glycolysis.
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The findings of this study suggest that inhibition of intracellular Ca(2+/-) overload could protect cells from damage and that VDAC1 plays a considerable role in Cr(VI)-induced liver injury.
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Our study suggested that miR-7 suppressed the expression of VDAC1 in hepatocellular carcinoma
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Results shows that beta-barrel of human VDAC1 embedded into a membrane is highly flexible and that Ca2+, a key regulator of metabolism and apoptosis, strongly decreases its plasticity suggesting that physiological VDAC function depends on the molecular plasticity of its channel.
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High VDAC1 expression is associated with cervical cancer.
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Studies using B16F10 and A375 cells genetically modified for ATF2 indicated that mitochondrial ATF2 was able to dissociate Bim from the Mcl-1/Bim complex to trigger VDAC1 oligomerization.
