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https://www.readbyqxmd.com/read/28618997/vdac1-as-a-player-in-mitochondria-mediated-apoptosis-and-target-for-modulating-apoptosis
#1
Varda Shoshan-Barmatz, Yakov Krelin, Quan Chen
The voltage-dependent anion channel 1 (VDAC1), an outer mitochondria membrane protein, functions as a mitochondrial governor, controlling transport of metabolites in and out of the mitochondria and energy production, while also coordinating glycolysis and oxidative phosphorylation (OXPHOS). . VDAC1 plays a key role in mitochondria-mediated apoptosis by functioning in the release of apoptotic proteins located in the inter-membranal space (IMS) and due to its association with pro- and anti-apoptotic proteins...
June 16, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28608415/crystal-structural-characterization-reveals-novel-oligomeric-interactions-of-human-voltage-dependent-anion-channel-1
#2
Toshiaki Hosaka, Masateru Okazaki, Tomomi Kimura-Someya, Yoshiko Ishizuka-Katsura, Kaori Ito, Shigeyuki Yokoyama, Kosuke Dodo, Mikiko Sodeoka, Mikako Shirouzu
Voltage-dependent anion channel 1 (VDAC1), which is located in the outer mitochondrial membrane, plays important roles in various cellular processes. For example, oligomerization of VDAC1 is involved in the release of cytochrome c to the cytoplasm, leading to apoptosis. However, it is unknown how VDAC1 oligomerization occurs in the membrane. In the present study, we determined high-resolution crystal structures of oligomeric human VDAC1 (hVDAC1) prepared by using an Escherichia coli cell-free protein synthesis system, which avoided the need for denaturation and refolding of the protein...
June 12, 2017: Protein Science: a Publication of the Protein Society
https://www.readbyqxmd.com/read/28592532/voltage-dependent-anion-channel-1-interacts-with-ribonucleoprotein-complexes-to-enhance-infectious-bursal-disease-virus-polymerase-activity
#3
Chunyan Han, Xiangwei Zeng, Shuai Yao, Li Gao, Lizhou Zhang, Xiaole Qi, Yulu Duan, Bo Yang, Yulong Gao, Changjun Liu, Yanping Zhang, Yongqiang Wang, Xiaomei Wang
Infectious bursal disease virus (IBDV) is a double-stranded RNA virus. Segment A contains two overlapping open reading frames (ORFs), which encode viral proteins VP2, VP3, VP4, and VP5. Segment B contains one ORF and encodes the viral RNA-dependent RNA polymerase, VP1. IBDV ribonucleoprotein complexes are composed of VP1, VP3, and dsRNA and play a critical role in mediating viral replication and transcription during virus life cycles. Here, we identified a cellular factor, VDAC1, which was upregulated during IBDV infection and found to mediate IBDV polymerase activity...
June 7, 2017: Journal of Virology
https://www.readbyqxmd.com/read/28571556/interactions-of-vdac-with-proteins-involved-in-neurodegenerative-aggregation-an-opportunity-for-advancement-on-therapeutic-molecules
#4
Andrea Magrì, Angela Messina
The Voltage Dependent Anion Channel (VDAC) proteins represent the most important pore-forming proteins of the mitochondrial outer membrane, directly involved in metabolism and apoptosis regulation. The recent literature has highlighted a key role of VDACs in mitochondrial dysfunction typical of many neurodegenerative disorders. In particular, the principal isoform VDAC1 represents the main mitochondrial docking site of many misfolded proteins, such as amyloid β and Tau in Alzheimer's disease, α-synuclein in Parkinson's disease and several SOD1 mutants in Amyotrophic Lateral Sclerosis...
May 31, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28554327/vdac-targeted-drugs-affecting-cytoprotection-and-mitochondrial-physiology-in-cerebrovascular-and-cardiovascular-diseases
#5
Andonis Karachitos, Joaquin Jordan, Hanna Kmita
Cerebrovascular and cardiovascular diseases are caused by impairment of the brain and/or heart circulation. Insufficient blood flow results in a decrease in oxygen delivery (ischemia) which affects mitochondria functioning and consequently lead to insufficient ATP production. Moreover, ischemia combined with the following reperfusion may result in further mitochondria dysfunction coexisting with lower ATP synthesis and higher ROS generation This, in turn, have direct implications in the pathogenesis of cerebrovascular and cardiovascular diseases...
May 29, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28554318/anti-cancer-compounds-targeted-to-vdac-potential-and-perspectives
#6
Simona Reina, Vito De Pinto
VDAC (Voltage-Dependent Anion selective Channel) is a small family of abundant pore-forming proteins located in the outer mitochondrial membrane. Their role range from the most intuitive, the formation of a hydrophilic conduit through the membrane thanks to its beta-barrel structure, to less understood functions that make them essential actors in the cross-talk between the bioenergetics metabolism and the cytosol components. Due to this localization, VDAC1, in particular, has been reported to be involved in apoptosis, hexokinase and tubulin binding, and in the Warburg effect...
May 29, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28501872/a-mechanism-study-underlying-the-protective-effects-of-cyclosporine-a-on-lung-ischemia-reperfusion-injury
#7
Jian''an Li, Zhongya Yan, Qianjin Fang
AIM: This study is aimed at validating the hypothesis that administration of cyclosporine-A (CsA) would be protective in lung ischemia-reperfusion (I/R) injury and in exploring the underlying mechanism. METHODS: Rabbits were divided into 4 groups: the control, sham operation, I/R, and I/R with CsA treatment. Flow cytometry was used to measure the mitochondrial membrane potential. Laser scanning confocal microscope was used to analyze mitochondrion permeability transition pore (MPTP)...
2017: Pharmacology
https://www.readbyqxmd.com/read/28483437/4-phenyl-butyric-acid-increases-particulate-hexokinase-activity-and-protects-against-ros-injury-in-l6-myotubes
#8
Michele Hinerasky da Silva, Flavia Letícia Martins Peçanha, Aline Machado de Oliveira, Wagner Seixas da-Silva
Hexokinase (HK) is the first enzyme in the glycolytic pathway and is responsible for glucose phosphorylation and fixation into the cell. HK (HK-II) is expressed in skeletal muscle and can be found in the cytosol or bound mitochondria, where it can protect cells against insults such as oxidative stress. 4-Phenyl butyric acid (4-PBA) is a chemical chaperone that inhibits endoplasmic reticulum stress and contributes to the restoring of glucose homeostasis. AIMS: Here, we decided to investigate whether HK activity and its interaction with mitochondria could be a target of 4-PBA action...
June 15, 2017: Life Sciences
https://www.readbyqxmd.com/read/28461778/expression-profile-of-mitochondrial-voltage-dependent-anion-channel-1-vdac1-influenced-genes-is-associated-with-pulmonary-hypertension
#9
Tong Zhou, Haiyang Tang, Ying Han, Dustin Fraidenburg, Young-Won Kim, Donghee Lee, Jeongyoon Choi, Hyoweon Bang, Jae-Hong Ko
Several human diseases have been associated with mitochondrial voltage-dependent anion channel-1 (VDAC1) due to its role in calcium ion transportation and apoptosis. Recent studies suggest that VDAC1 may interact with endothelium-dependent nitric oxide synthase (eNOS). Decreased VDAC1 expression may limit the physical interaction between VDAC1 and eNOS and thus impair nitric oxide production, leading to cardiovascular diseases, including pulmonary arterial hypertension (PAH). In this report, we conducted meta-analysis of genome-wide expression data to identify VDAC1 influenced genes implicated in PAH pathobiology...
May 2017: Korean Journal of Physiology & Pharmacology
https://www.readbyqxmd.com/read/28449397/differential-proteome-profiling-in-the-hippocampus-of-amnesic-mice
#10
Meghraj Singh Baghel, Mahendra Kumar Thakur
Amnesia or memory loss is associated with brain aging and several neurodegenerative pathologies including Alzheimer's disease (AD). This can be induced by a cholinergic antagonist scopolamine but the underlying molecular mechanism is poorly understood. This study of proteome profiling in the hippocampus could provide conceptual insights into the molecular mechanisms involved in amnesia. To reveal this, mice were administered scopolamine to induce amnesia and memory impairment was validated by novel object recognition test...
April 27, 2017: Hippocampus
https://www.readbyqxmd.com/read/28443244/the-mitochondrial-voltage-dependent-anion-channel-1-ca-2-transport-apoptosis-and-their-regulation
#11
REVIEW
Varda Shoshan-Barmatz, Soumasree De, Alon Meir
In the outer mitochondrial membrane, the voltage-dependent anion channel 1 (VDAC1) functions in cellular Ca(2+) homeostasis by mediating the transport of Ca(2+) in and out of mitochondria. VDAC1 is highly Ca(2+)-permeable and modulates Ca(2+) access to the mitochondrial intermembrane space. Intramitochondrial Ca(2+) controls energy metabolism by enhancing the rate of NADH production via modulating critical enzymes in the tricarboxylic acid cycle and fatty acid oxidation. Mitochondrial [Ca(2+)] is regarded as an important determinant of cell sensitivity to apoptotic stimuli and was proposed to act as a "priming signal," sensitizing the organelle and promoting the release of pro-apoptotic proteins...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/28431142/respiratory-chain-enzyme-deficiency-induces-mitochondrial-location-of-actin-binding-gelsolin-to-modulate-the-oligomerization-of-vdac-complexes-and-cell-survival
#12
Alberto García-Bartolomé, Ana Peñas, Lorena Marín-Buera, Teresa Lobo-Jarne, Rafael Pérez-Pérez, María Morán, Joaquín Arenas, Miguel A Martín, Cristina Ugalde
Despite considerable knowledge on the genetic basis of mitochondrial disorders, their pathophysiological consequences remain poorly understood. We previously used 2D-DIGE analyses to define a protein profile characteristic for respiratory chain complex III-deficiency that included a significant overexpression of cytosolic Gelsolin (GSN), a cytoskeletal protein that regulates the severing and capping of the actin filaments. Biochemical and immunofluorescence assays confirmed a specific increase of GSN levels in the mitochondria from patientś fibroblasts and from transmitochondrial cybrids with complex III assembly defects...
April 18, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28412744/mitochondrial-vdac1-based-peptides-attacking-oncogenic-properties-in-glioblastoma
#13
Anna Shteinfer-Kuzmine, Tasleem Arif, Yakov Krelin, Shambhoo Sharan Tripathi, Avijit Paul, Varda Shoshan-Barmatz
Glioblastoma multiforme (GBM), a primary brain malignancy characterized by high morbidity, invasiveness, proliferation, relapse and mortality, is resistant to chemo- and radiotherapies and lacks effective treatment. GBM tumors undergo metabolic reprograming and develop anti-apoptotic defenses. We targeted GBM with a peptide derived from the mitochondrial protein voltage-dependent anion channel 1 (VDAC1), a key component of cell energy, metabolism and apoptosis regulation. VDAC1-based cell-penetrating peptides perturbed cell energy and metabolic homeostasis and induced apoptosis in several GBM and GBM-derived stem cell lines...
May 9, 2017: Oncotarget
https://www.readbyqxmd.com/read/28398674/melatonin-protects-cardiac-microvasculature-against-ischemia-reperfusion-injury-via-suppression-of-mitochondrial-fission-vdac1-hk2-mptp-mitophagy-axis
#14
Hao Zhou, Ying Zhang, Shunying Hu, Chen Shi, Pingjun Zhu, Qiang Ma, Qinhua Jin, Feng Cao, Feng Tian, Yundai Chen
The cardiac microvascular system, which is primarily composed of monolayer endothelial cells, is the site of blood supply and nutrient exchange to cardiomyocytes. However, microvascular ischemia/reperfusion injury (IRI) following percutaneous coronary intervention is a woefully neglected topic and few strategies are available to reverse such pathologies. Here, we studied the effects of melatonin on microcirculation IRI and elucidated the underlying mechanism. Melatonin markedly reduced infarcted area, improved cardiac function, restored blood flow and lower microcirculation perfusion defects...
April 11, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28396346/photoaffinity-labeling-with-cholesterol-analogues-precisely-maps-a-cholesterol-binding-site-in-voltage-dependent-anion-channel-1
#15
Melissa M Budelier, Wayland W L Cheng, Lucie Bergdoll, Zi-Wei Chen, James W Janetka, Jeff Abramson, Kathiresan Krishnan, Laurel Mydock-McGrane, Douglas F Covey, Julian P Whitelegge, Alex S Evers
Voltage-dependent anion channel-1 (VDAC1) is a highly regulated β-barrel membrane protein that mediates transport of ions and metabolites between the mitochondria and cytosol of the cell. VDAC1 co-purifies with cholesterol and is functionally regulated by cholesterol, among other endogenous lipids. Molecular modeling studies based on NMR observations have suggested five cholesterol-binding sites in VDAC1, but direct experimental evidence for these sites is lacking. Here, to determine the sites of cholesterol binding, we photolabeled purified mouse VDAC1 (mVDAC1) with photoactivatable cholesterol analogues and analyzed the photolabeled sites with both top-down mass spectrometry (MS), and bottom-up MS paired with a clickable, stable isotope-labeled tag, FLI-tag...
June 2, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28393069/commentary-synthetic-ubiquinones-specifically-bind-to-mitochondrial-voltage-dependent-anion-channel-1-vdac1-in-saccharomyces-cerevisiae-mitochondria
#16
COMMENT
Manuel Gutiérrez-Aguilar
No abstract text is available yet for this article.
2017: Frontiers in Molecular Biosciences
https://www.readbyqxmd.com/read/28343033/quinocetone-induces-mitochondrial-apoptosis-in-hepg2-cells-through-ros-dependent-promotion-of-vdac1-oligomerization-and-suppression-of-wnt1-%C3%AE-catenin-signaling-pathway
#17
Xiayun Yang, Shusheng Tang, Chongshan Dai, Daowen Li, Shen Zhang, Sijun Deng, Yan Zhou, Xilong Xiao
Quinocetone (QCT) has been used as an animal feed additive in China since 2003. However, investigations indicate that QCT has potential toxicity due to the fact that it shows cytotoxicity, genotoxicity, hepatotoxicity, nephrotoxicity and immunotoxicity in vitro and animal models. Although QCT-induced mitochondrial apoptosis has been established, the molecular mechanism remains unclear. This study was aimed to investigate the role of voltage-dependent anion channel 1 (VDAC1) oligomerization and Wnt/β-catenin pathway in QCT-induced mitochondrial apoptosis...
March 23, 2017: Food and Chemical Toxicology
https://www.readbyqxmd.com/read/28339833/vdac1-is-a-molecular-target-in-glioblastoma-with-its-depletion-leading-to-reprogrammed-metabolism-and-reversed-oncogenic-properties
#18
Tasleem Arif, Yakov Kerlin, Itay Nakdimon, Daniel Benharroch, Avijit Paul, Daniela Dadon-Klein, Varda Shoshan-Barmatz
Background.: Glioblastoma (GBM), an aggressive brain tumor with frequent relapses and a high mortality, still awaits an effective treatment. Like many cancers, GBM cells acquire oncogenic properties, including metabolic reprogramming, vital for growth. As such, tumor metabolism is an emerging avenue for cancer therapy. One relevant target is the voltage-dependent anion channel 1 (VDAC1), a mitochondrial protein controlling cell energy and metabolic homeostasis. Methods...
February 28, 2017: Neuro-oncology
https://www.readbyqxmd.com/read/28327594/aspirin-induces-cell-death-by-directly-modulating-mitochondrial-voltage-dependent-anion-channel-vdac
#19
Debanjan Tewari, Dhriti Majumdar, Sirisha Vallabhaneni, Amal Kanti Bera
Aspirin induces apoptotic cell death in various cancer cell lines. Here we showed that silencing of VDAC1 protected HeLa cells from aspirin-induced cell death. Compared to the wild type cells, VDAC1 knocked down cells showed lesser change of mitochondrial membrane potential (Δψm), upon aspirin treatment. Aspirin augmented ATP and ionomycin-induced mitochondrial Ca(2+) uptake which was abolished in VDAC1 knocked down cells. Aspirin dissociated bound hexokinase II (HK-II) from mitochondria. Further, aspirin promoted the closure of recombinant human VDAC1, reconstituted in planar lipid bilayer...
March 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28288978/mff-dependent-mitochondrial-fission-contributes-to-the-pathogenesis-of-cardiac-microvasculature-ischemia-reperfusion-injury-via-induction-of-mros-mediated-cardiolipin-oxidation-and-hk2-vdac1-disassociation-involved-mptp-opening
#20
Hao Zhou, Shunying Hu, Qinhua Jin, Chen Shi, Ying Zhang, Pingjun Zhu, Qiang Ma, Feng Tian, Yundai Chen
BACKGROUND: The cardiac microvascular system ischemia/reperfusion injury following percutaneous coronary intervention is a clinical thorny problem. This study explores the mechanisms by which ischemia/reperfusion injury induces cardiac microcirculation collapse. METHODS AND RESULTS: In wild-type mice, mitochondrial fission factor (Mff) expression increased in response to acute microvascular ischemia/reperfusion injury. Compared with wild-type mice, homozygous Mff-deficient (Mff(gt)) mice exhibited a smaller infarcted area, restored cardiac function, improved blood flow, and reduced microcirculation perfusion defects...
March 13, 2017: Journal of the American Heart Association
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