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https://www.readbyqxmd.com/read/28096195/the-multifunctional-mitochondrial-epac1-controls-myocardial-cell-death
#1
Loubina Fazal, Marion Laudette, Sílvia Paula-Gomes, Sandrine Pons, Caroline Conte, Florence Tortosa, Pierre Sicard, Yannis Sainte-Marie, Malik Bisserier, Olivier Lairez, Alexandre Lucas, Jérôme Roy, Bijan Ghaleh, Jeremy Fauconnier, Jeanne Mialet-Perez, Frank Lezoualc'h
RATIONALE: Although the second messenger cyclic AMP (cAMP) is physiologically beneficial in the heart, it largely contributes to cardiac disease progression when dysregulated. Current evidence suggests that cAMP is produced within mitochondria. However, mitochondrial cAMP signaling and its involvement in cardiac pathophysiology are far from being understood. OBJECTIVE: To investigate the role of mitochondrial exchange protein directly activated by cAMP 1 (MitEpac1) in ischemia/reperfusion (I/R) injury...
January 17, 2017: Circulation Research
https://www.readbyqxmd.com/read/28060261/study-of-endoplasmic-reticulum-and-mitochondria-interactions-by-in-situ-proximity-ligation-assay-in-fixed-cells
#2
Emily Tubbs, Jennifer Rieusset
Structural interactions between the endoplasmic reticular (ER) and mitochondrial membranes, in domains known as mitochondria-associated membranes (MAM), are crucial hubs for cellular signaling and cell fate. Particularly, these inter-organelle contact sites allow the transfer of calcium from the ER to mitochondria through the voltage-dependent anion channel (VDAC)/glucose-regulated protein 75 (GRP75)/inositol 1,4,5-triphosphate receptor (IP3R) calcium channeling complex. While this subcellular compartment is under intense investigation in both physiological and pathological conditions, no simple and sensitive method exists to quantify the endogenous amount of ER-mitochondria contact in cells...
December 10, 2016: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/28051849/synthetic-ubiquinones-specifically-bind-to-mitochondrial-voltage-dependent-anion-channel-1-vdac1-in-saccharomyces-cerevisiae-mitochondria
#3
Masatoshi Murai, Ayaka Okuda, Takenori Yamamoto, Yasuo Shinohara, Hideto Miyoshi
The role of voltage-dependent anion channel (VDAC) as a metabolic gate of the mitochondrial outer membrane has been firmly established; however, its involvement in the regulation of mitochondrial permeability transition (PT) remains extremely controversial. Although some low-molecular-weight chemicals have been proposed to modulate the regulatory role of VDAC in the induction of PT, direct binding between these chemicals and VDAC has not yet been demonstrated. In the present study, we investigated whether the ubiquinone molecule directly binds to VDAC in Saccharomyces cerevisiae mitochondria through a photoaffinity labeling technique using two photoreactive ubiquinones (PUQ-1 and PUQ-2)...
January 4, 2017: Biochemistry
https://www.readbyqxmd.com/read/28028442/regulation-of-vdac-trafficking-modulates-cell-death
#4
Ashvini K Dubey, Ashwini Godbole, M K Mathew
The voltage-dependent anion channel (VDAC) and mitochondria-associated hexokinase (HxK) have crucial roles in both cell survival and death. Both the individual abundances and their ratio seem to influence the balance of survival and death and are thus critical in scenarios, such as neurodegeneration and cancer. Elevated levels of both VDAC and HxK have been reported in cancerous cells. Physical interaction is surmised and specific residues or regions involved have been identified, but details of the interaction and the mechanism by which it modulates survival are yet to be elucidated...
2016: Cell Death Discovery
https://www.readbyqxmd.com/read/27989743/high-resolution-mass-spectrometry-characterization-of-the-oxidation-pattern-of-methionine-and-cysteine-residues-in-rat-liver-mitochondria-voltage-dependent-anion-selective-channel-3-vdac3
#5
Rosaria Saletti, Simona Reina, Maria G G Pittalà, Ramona Belfiore, Vincenzo Cunsolo, Angela Messina, Vito De Pinto, Salvatore Foti
Voltage-dependent anion selective channels (VDACs) are integral membrane proteins found in the mitochondrial outer membrane. In comparison with the most abundant isoform VDAC1, there is little knowledge about the functional role of VDAC3. Unlikely VDAC1, cysteine residues are particularly abundant in VDAC3. Since the mitochondrial intermembrane space (IMS) has an oxidative potential we questioned whether the redox state of VDAC3 can be modified. By means of SDS-PAGE separation, tryptic and chymotryptic proteolysis and UHPLC/High Resolution ESI-MS/MS analysis we investigated the oxidation state of cysteine and methionine residues of rat liver VDAC3...
December 16, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27988168/dna-methylation-and-histone-deacetylation-regulating-insulin-sensitivity-due-to-chronic-cold-exposure
#6
Xiaoqing Wang, Lai Wang, Yizheng Sun, Ruiping Li, Jinbo Deng, Jiexin Deng
In this study, we investigated the causal relationship between chronic cold exposure and insulin resistance and the mechanisms of how DNA methylation and histone deacetylation regulate cold-reduced insulin resistance. 46 adult male mice from postnatal day 90-180 were randomly assigned to control group and cold-exposure group. Mice in cold-exposure group were placed at temperature from -1 to 4 °C for 30 days to mimic chronic cold environment. Then, fasting blood glucose, blood insulin level and insulin resistance index were measured with enzymatic methods...
December 14, 2016: Cryobiology
https://www.readbyqxmd.com/read/27941998/voltage-dependent-anion-channel-1-vdac1-participates-the-apoptosis-of-the-mitochondrial-dysfunction-in-desminopathy
#7
Huanyin Li, Lan Zheng, Yanqing Mo, Qi Gong, Aihua Jiang, Jing Zhao
Desminopathies caused by the mutation in the gene coding for desmin are genetically protein aggregation myopathies. Mitochondrial dysfunction is one of pathological changes in the desminopathies at the earliest stage. The molecular mechanisms of mitochondria dysfunction in desminopathies remain exclusive. VDAC1 regulates mitochondrial uptake across the outer membrane and mitochondrial outer membrane permeabilization (MOMP). Relationships between desminopathies and Voltage-dependent anion channel 1 (VDAC1) remain unclear...
2016: PloS One
https://www.readbyqxmd.com/read/27909249/mortalin-mediated-and-erk-controlled-targeting-of-hif-1%C3%AE-to-mitochondria-confers-resistance-to-apoptosis-under-hypoxia
#8
Ilias Mylonis, Maria Kourti, Martina Samiotaki, George Panayotou, George Simos
Hypoxia inducible factor-1 (HIF-1) is the main transcriptional activator of the cellular response to hypoxia and an important target of anticancer therapy. Phosphorylation by ERK stimulates the transcriptional activity of HIF-1α by inhibiting its CRM1-dependent nuclear export. Here, we demonstrate that phosphorylation by ERK also regulates the association of HIF-1α with a novel interaction partner identified as mortalin (GRP75) which mediates non-genomic involvement of HIF-1α in apoptosis. Mortalin binds specifically to HIF-1α lacking modification by ERK and their complex is localized outside the nucleus...
December 1, 2016: Journal of Cell Science
https://www.readbyqxmd.com/read/27898307/a-ca-2-chelator-ameliorates-chromium-vi-induced-hepatocyte-l-02-injury-via-down-regulation-of-voltage-dependent-anion-channel-1-vdac1-expression
#9
Xing Yi, Fang Xiao, Xiali Zhong, Yujie Duan, Kaihua Liu, Caigao Zhong
Hexavalent chromium could result in cell malfunctions. Intracellular Ca(2+) ([Ca(2+)]i) content and VDAC1 expression are both important features related to cell survial. This study aimed to explore the mechanism of cell injury induced by Cr(VI) and tentatively offer clues to repairing this cell damage using [Ca(2+)]i and VDAC1. L-02 hepatocytes were treated with Cr(VI)/BAPTA, and the levels of [Ca(2+)]i and cell injury associated with Cr(VI) were determined in addition to the effect of BAPTA. The expression of VDAC1 in Cr(VI)-induced cells was evaluated...
November 18, 2016: Environmental Toxicology and Pharmacology
https://www.readbyqxmd.com/read/27894242/indazolo-3-2-b-quinazolinones-attack-hepatocellular-carcinoma-hep3b-cells-by-inducing-mitochondrial-dependent-apoptosis-and-inhibition-of-nrf2-are-signaling-pathway
#10
Y Zhang, R Qiao, D He, Z Zhao, S Yang, H Zou, X Zhang, M Wu, J Chen, P Chen
Hepatocellular carcinoma (HCC) is the second leading cause of cancer death worldwide. Genotoxic stress resistance in patients often contributes to poor clinical outcomes, and is intensively associated to the upregulation of Nrf2/ARE signaling pathway. In this study, we examined the connection between the anti-cancer activity of two novel indazolo[3,2-b]quinazolinone (IQ) derivatives, IQ-7 and IQ-12, and their effect on the Nrf2/ARE signaling pathway. The two compounds were shown to induce apoptosis and inhibit the Nrf2/ARE signaling pathway in Hep3B cells (human hepatoma cell line)...
November 28, 2016: Current Molecular Medicine
https://www.readbyqxmd.com/read/27891320/the-association-of-vdac-with-cell-viability-of-pc12-model-of-huntington-s-disease
#11
Andonis Karachitos, Daria Grobys, Klaudia Kulczyńska, Adrian Sobusiak, Hanna Kmita
It is becoming increasingly apparent that mitochondria dysfunction plays an important role in the pathogenesis of Huntington's disease (HD), but the underlying mechanism is still elusive. Thus, there is a still need for further studies concerning the upstream events in the mitochondria dysfunction that could contribute to cell death observed in HD. Taking into account the fundamental role of the voltage-dependent anion-selective channel (VDAC) in mitochondria functioning, it is reasonable to consider the channel as a crucial element in HD etiology...
2016: Frontiers in Oncology
https://www.readbyqxmd.com/read/27859782/inhibition-of-the-mitochondrial-calcium-uniporter-rescues-dopaminergic-neurons-in-pink1-zebrafish
#12
Smijin Soman, Marcus Keatinge, Mahsa Moein, Marc Da Costa, Heather Mortiboys, Alexander Skupin, Sreedevi Sugunan, Michal Bazala, Jacek Kuznicki, Oliver Bandmann
Mutations in PTEN-induced putative kinase 1 (PINK1) are a cause of early onset Parkinson's disease (PD). Loss of PINK1 function causes dysregulation of mitochondrial calcium homeostasis, resulting in mitochondrial dysfunction and neuronal cell death. We report that both genetic and pharmacological inactivation of the mitochondrial calcium uniporter (MCU), located in the inner mitochondrial membrane, prevents dopaminergic neuronal cell loss in pink1(Y431) * mutant zebrafish (Danio rerio) via rescue of mitochondrial respiratory chain function...
November 12, 2016: European Journal of Neuroscience
https://www.readbyqxmd.com/read/27816759/brain-quantitative-proteomic-responses-reveal-new-insight-of-benzotriazole-neurotoxicity-in-female-chinese-rare-minnow-gobiocypris-rarus
#13
Xuefang Liang, Christopher J Martyniuk, Jinmiao Zha, Zijian Wang
Benzotriazole (BT) is a high-production volume chemical which has been ubiquitously detected in aquatic environments. Although adverse effects from acute and chronic exposure to BT have been reported, the neurotoxic effect of BT and the mechanisms of toxicity are not well documented. In this study, adult female Chinese rare minnow (Gobiocypris rarus) were exposed to 0.05, 0.5, and 5mg/L BT for 28days. The brain proteome showed that BT exposure mainly involved in metabolic process, signal transduction, stress response, cytoskeleton, and transport...
December 2016: Aquatic Toxicology
https://www.readbyqxmd.com/read/27814578/lipid-raft-er-signalosome-malfunctions-in-menopause-and-alzheimer-s-disease
#14
Ana Canerina-Amaro, Luis G Hernandez-Abad, Isidre Ferrer, David Quinto-Alemany, Fatima Mesa-Herrera, Carla Ferri, Ricardo A Puertas-Avendano, Mario Diaz, Raquel Marin
The increase in the incidence of Alzheimer's disease (AD) in old women may be attributable to estrogen deficiency, and estrogen replacement therapy may be useful in preventing or delaying the onset of this disease. In neuronal membranes, 17 beta-estradiol interacts with estrogen receptors (mERs) located in lipid raft signalosomes which trigger neuroprotective responses by anchoring to scaffolding caveolin-1 complexed with other proteins. We suggest that mER-signalosome malfunctions in AD and by menopause due to development of aberrations in these microstructures...
January 1, 2017: Frontiers in Bioscience (Scholar Edition)
https://www.readbyqxmd.com/read/27796346/lncrna-h19-mir-675-axis-regulates-cardiomyocyte-apoptosis-by-targeting-vdac1-in-diabetic-cardiomyopathy
#15
Xiangquan Li, Hao Wang, Biao Yao, Weiting Xu, Jianchang Chen, Xiang Zhou
We previously established a rat model of diabetic cardiomyopathy (DCM) and found that the expression of lncRNA H19 was significantly downregulated. The present study was designed to investigate the pathogenic role of H19 in the development of DCM. Overexpression of H19 in diabetic rats attenuated oxidative stress, inflammation and apoptosis, and consequently improved left ventricular function. High glucose was associated with reduced H19 expression and increased cardiomyocyte apoptosis. To explore the molecular mechanisms involved, we performed in vitro experiments using cultured neonatal rat cardiomyocytes...
October 31, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27778231/identification-of-potential-predictive-markers-of-dexamethasone-resistance-in-childhood-acute-lymphoblastic-leukemia
#16
Nasrin Dehghan-Nayeri, Mostafa Rezaei-Tavirani, Mir Davood Omrani, Ahmad Gharehbaghian, Kourosh Goudarzi Pour, Peyman Eshghi
Response to dexamethasone (DEXA), as a hallmark drug in the treatment of childhood acute lymphoblastic leukemia (ALL), is one of the pivotal prognostic factors in the prediction of outcome in ALL. Identification of predictive markers of chemoresistance is beneficial to selecting of the best therapeutic protocol with the lowest effect adverse. Hence, we aimed to find drug targets using the 2DE/MS proteomics study of a DEXA-resistant cell line (REH) as a model for poor DEXA responding patients before and after drug treatment...
October 24, 2016: Journal of Cell Communication and Signaling
https://www.readbyqxmd.com/read/27761954/novel-insights-into-role-of-mir-320a-vdac1-axis-in-astrocyte-mediated-neuronal-damage-in-neuroaids
#17
Mahar Fatima, Bharat Prajapati, Kanza Saleem, Rina Kumari, Chitra Mohindar Singh Singal, Pankaj Seth
Astroglia are indispensable component of the tripartite synapse ensheathing innumerous soma and synapses. Its proximity to neurons aids the regulation of neuronal functions, health and survival through dynamic neuroglia crosstalk. Susceptibility of astrocyte to HIV-1 infection and subsequent latency culminates in compromised neuronal health. The viral protein HIV-1 transactivator of transcription (Tat) is neurotoxic. HIV-1 Tat is detected in brain of AIDS patients even in cases where viral load is non-detectable due to successful HAART therapy...
February 2017: Glia
https://www.readbyqxmd.com/read/27738100/novel-compounds-targeting-the-mitochondrial-protein-vdac1-inhibit-apoptosis-and-protect-against-mitochondrial-dysfunction
#18
Danya Ben-Hail, Racheli Begas-Shvartz, Moran Shalev, Anna Shteinfer-Kuzmine, Arie Gruzman, Simona Reina, Vito De Pinto, Varda Shoshan-Barmatz
Apoptosis is thought to play a critical role in several pathological processes, such as neurodegenerative diseases (i.e. Parkinson's and Alzheimer's diseases) and various cardiovascular diseases. Despite the fact that apoptotic mechanisms are well defined, there is still no substantial therapeutic strategy to stop or even slow this process. Thus, there is an unmet need for therapeutic agents that are able to block or slow apoptosis in neurodegenerative and cardiovascular diseases. The outer mitochondrial membrane protein voltage-dependent anion channel 1 (VDAC1) is a convergence point for a variety of cell survival and death signals, including apoptosis...
November 25, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27721436/hexokinase-i-n-terminal-based-peptide-prevents-the-vdac1-sod1-g93a-interaction-and-re-establishes-als-cell-viability
#19
Andrea Magrì, Ramona Belfiore, Simona Reina, Marianna Flora Tomasello, Maria Carmela Di Rosa, Francesca Guarino, Loredana Leggio, Vito De Pinto, Angela Messina
Superoxide Dismutase 1 mutants associate with 20-25% of familial Amyotrophic Lateral Sclerosis (ALS) cases, producing toxic aggregates on mitochondria, notably in spinal cord. The Voltage Dependent Anion Channel isoform 1 (VDAC1) in the outer mitochondrial membrane is a docking site for SOD1 G93A mutant in ALS mice and the physiological receptor of Hexokinase I (HK1), which is poorly expressed in mouse spinal cord. Our results demonstrate that HK1 competes with SOD1 G93A for binding VDAC1, suggesting that in ALS spinal cord the available HK1-binding sites could be used by SOD1 mutants for docking mitochondria, producing thus organelle dysfunction...
October 10, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27677502/protein-coingestion-with-alcohol-following-strenuous-exercise-attenuates-alcohol-induced-intramyocellular-apoptosis-and-inhibition-of-autophagy
#20
William J Smiles, Evelyn B Parr, Vernon G Coffey, Orly Lacham-Kaplan, John A Hawley, Donny M Camera
Alcohol ingestion decreases post-exercise rates of muscle protein synthesis, but the mechanism(s) (e.g., increased protein breakdown) underlying this observation are unknown. Autophagy is an intracellular "recycling" system required for homeostatic substrate and organelle turnover; its dysregulation may provoke apoptosis and lead to muscle atrophy. We investigated the acute effects of alcohol ingestion on autophagic cell signaling responses to a bout of concurrent (combined resistance- and endurance-based) exercise...
September 27, 2016: American Journal of Physiology. Endocrinology and Metabolism
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