anti-Voltage-Dependent Anion Channel 1 (VDAC1) Antibodies

Arabidopsis thaliana Voltage-Dependent Anion Channel 1 (VDAC1) interaction partners

1. Abnormal ovules in the process of female gametogenesis were observed. Both mitochondrial transmembrane potential and ATP synthesis rate were obviously reduced in the mitochondria isolated from atvdac1 plants.

2. Data indicate that both voltage-dependent anion channel 1 (AtVDAC1) and calcium sensor CBL1 regulate cold stress responses during seed germination and plant development.

3. AtVDAC1 has a main function in mitochondria

4. VDAC1 is not only necessary for normal growth but also important for disease resistance through regulation of hydrogen peroxide generation.

Human Voltage-Dependent Anion Channel 1 (VDAC1) interaction partners

1. findings implied that because of its interactions with VDAC-1, the cryptic MBP84-104 peptide invoked reprogramming of the cellular energy metabolism that favored enhanced cellular activity, rather than apoptotic cell death.

2. The inactivation of VDAC-1 function either by pharmacological means or siRNA lead to significant decrease of Mycobacterium avium survival.

3. The focus of this review is the involvement of mitochondrial dysfunction in Alzheimer's disease, and specifically, the role of the voltage-dependent anion channel 1 (VDAC1), which has been linked to Alzheimer's disease pathogenesis. [review]

4. 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.

5. associate dysfunction in Fe-S cluster biogenesis with cleavage of VDAC1

6. 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.

7. 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.

8. VDAC1 plays an important role in dengue virus infection.

9. 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

10. The results of this study shown VDAC1, the Potential Target of miR-320a, is Upregulated in Response to HIV-1 Tat.

11. the present study indicated that VDAC1 may interact with HPV16 E7 to promote the malignant progression of HPV-related cervical cancer

12. Porin expression was lower in patients with heart failure with preserved ejection fraction compared to controls.

13. Studied voltage-dependent anion channel 1 (VDAC1) structure and oligomerization using an Escherichia coli cell-free protein synthesis system and bicelle crystallization.

14. 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.

15. VDAC1 was accumulated in the desmin highly stained area of muscle fibers of desminopathy patients.

16. 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.

17. 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.

18. 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.

19. 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.

20. Our study suggested that miR-7 suppressed the expression of VDAC1 in hepatocellular carcinoma

Pig (Porcine) Voltage-Dependent Anion Channel 1 (VDAC1) interaction partners

1. Data confirm the synthesis of VDAC1 and 2 subtypes in GV (germinal vesicle) and MII (meiosis II) stage porcine oocytes as well as their protein expression.

Cow (Bovine) Voltage-Dependent Anion Channel 1 (VDAC1) interaction partners

1. Results describe the expression of voltage-dependent anion channel isoforms in rat, bovine, and chicken brain mitochondria, and suggest that the nature of hexokinase binding site is not determined by the expression of a single VDAC isoform.

2. Suggest that VDAC1 participates in volume regulatory processes in spermatozoa.

Mouse (Murine) Voltage-Dependent Anion Channel 1 (VDAC1) interaction partners

1. This study presents the structure of Vdac1-tethered bilayer lipid membranes determined using neutron reflectivity.

2. These results suggest a critical role for VDAC1 in mitochondrial fragmentation and its potential therapeutic value against glutamate-mediated oxidative neurotoxicity.

3. The VDAC1-based peptide R-Tf-D-LP4 has multiple effects on liver cancer cells.

4. Data indicate a specific pH-dependent dimerization of murine voltage-dependent anion channel 1 (mVDAC1).

5. Studied melatonin's role in microvascular ischemia/reperfusion injury; found melatonin plays a protective role in mitochondrial fission-VDAC1-HK2-mPTP-mitophagy axis signal pathway suppression.

6. microcirculatory ischemia/reperfusion injury can be attributed to Mff-dependent mitochondrial fission via voltage-dependent anion channel 1/hexokinase 2-mediated mitochondrial permeability transition pore opening and mitochondrial reactive oxygen species/cardiolipin involved cyt-c release.

7. This study demonstrated that Vdac1 was significantly downregulated in amnesic mice and showed interaction with other proteins in interaction network.

8. 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.

9. 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.

10. In cornu ammonis 1 region astrocytes, increasing miR-29a decreased VDAC1 and improved cell survival, while knockdown of VDAC1 improved survival.

11. VDAC1-interacting anion transport inhibitors inhibited apoptosis via direct interaction with VDAC1 to inhibit its oligomerization and subsequent Cyto c release and apoptosis.

12. Reducing VDAC1 expression induces a non-apoptotic role for pro-apoptotic proteins in glioblastoma multiforme cancer cell differentiation.

13. TSPO as a novel element in the regulation of mitochondrial quality control by autophagy, and demonstrate the importance for cell homeostasis of its expression ratio with voltage-dependent anion channel 1

14. ATP flows through VDAC through multiple pathways, in agreement with our structural data and experimentally determined physiological rates.

15. Reduced VDAC1 expression protects against Alzheimer's disease and synaptic deficiencies.

16. Data suggest presence of unstructured C-terminal tubulin tail in VDAC pore decreases conductance and switches selectivity from anionic to cationic rendering ATP transport virtually impossible; involves stable salt bridge (K336-tubulin/D186-Vdac1).

17. MAVS binds to voltage-dependent anion channel 1 (VDAC1) and induces apoptosis by caspase-3 activation, which is independent of its role in innate immunity.

18. Abnormal interaction of VDAC1 with amyloid beta and phosphorylated tau causes mitochondrial dysfunction in Alzheimer's disease.

19. Flexibility of the N-terminal mVDAC1 segment controls the channel's gating behavior.

20. the N-terminal alpha-helix is located inside the pore of VDAC in the open state and remains associated with beta-strand 11 of the pore wall during voltage gating

Zebrafish Voltage-Dependent Anion Channel 1 (VDAC1) interaction partners

1. we found that Bcl-wav controls intracellular Ca(2+) trafficking by acting on the mitochondrial voltage-dependent anion channel, and possibly on MCU, with direct consequences on actin microfilament dynamics and blastomere migration guidance.