Similar Datasets
Project description:Voltage dependent anion channel 1 (VDAC1) is a multi-functional protein that regulates mitochondrial membrane potential, calcium regulation, and apoptosis. VDAC1 also interacts with a number of signaling pathways important for energy homeostasis and proteins involved in neurodegenerative diseases such as alpha-synuclein. To identify novel signaling pathways dependent upon VDAC1 protein in dopamine cells, we used CRISPR-Cas9 gene editing in rat immortalized dopaminergic N27 cells. Western blot confirmed that VDAC1 protein levels were reduced ~90%. Mitochondrial bioenergetics was assessed to determine if there was functional loss of mitochondrial function without VDAC1. Loss of VDAC1 resulted in lower ATP-linked and maximum respiration, and spare respiratory capacity. Transcriptomics was conducted in these cells to identify the pathways perturbed by loss of VDAC. This study sheds novel insight into the different regulatory roles mediated by VDAC1 in dopamine cells.
2019-07-31 | GSE118737 | GEO
Project description:Our previous study has shown that the expression of voltage-dependent anion channel 1 (VDAC1) is closely related to the tumorigenesis and progression of HCC.Nevertheless, tumorigenesis and progression of HCC are complex processes, and the specific mechanism of VDAC1 affecting the proliferation and invasion of HCC has not yet been elucidated. To further study the role of downstream related molecules of VDAC1, we utilized the Affymetrix GeneChip system to analyze the downstream gene expression profile of VDAC1
2022-05-23 | GSE198538 | GEO
Project description:U87 xenograft tumors treated with scrambled siRNA (Tas_73, Tas_78) or siRNA against VDAC1 (Tas_57, Tas_61) We used microarrays to detail the global effect of siRNA against VDAC1 on subcotenous xenograft U87 cells tumors
2016-02-01 | GSE73243 | GEO
Project description:Mitochondria are subcellular organelles that are more than just the powerhouse of cells, they also dictate if a cell dies or survives. The mitochondrial outer-membrane voltage-dependent anion channel 1 (VDAC1) has been shown to play a crucial role in metabolism and apoptosis, however its involvement in ischemic pathologies and cancer is not clear. Transcriptome analysis of Vdac1-/- mouse embryonic fibroblasts (MEF) highlighted cancer and inflammation as top diesases but also activation of the HIF-1 signaling pathway in normoxia. HIF-1α protein was stable due to ROS accumulation that decreased respiration and glycolysis and maintained basal apoptosis. However, in hypoxia increased activation of ERK in combination with maintenance of respiration and increased glycolysis counterbalanced the deleterious effects of ROS, thereby allowing Vdac1-/- MEF to proliferate better than wild-type MEF. Xenografts of RAS-transformed Vdac1-/- MEF in mice showed stabilization of both HIF-1α and HIF-2α which led to blood vessel destabilization and a strong inflammatory response. Moreover, expression of Cdkn2a, a HIF-1-target and tumor suppressor gene, was strongly decreased. Consequently RAS-transformed Vdac1-/- MEF tumors grew faster than wild-type MEF tumors. These findings provide new perspectives into the understanding of VDAC1 in the function of mitochondria not only in cancer but also in inflammatory diseases. Profiling of VDAC1-/- and wild-type (Wt) Mouse Embryonic Fibroblasts (MEFs) was performed using whole genome mouse microarrays. in normoxic or hypoxic conditions. MEF (Wt and Vdac1-/-) were incubated in normoxia (Nx, ie: 20% O2) or hypoxia (Hx, ie: 1% O2) for 72h and then lysed prior to RNA isolation, labelling and hybridization on microarrays. One color experiment with 2 biological replicates (marked 1 or 2) of the 4 experimental conditions. One condition (MEF WT Nx2) has been removed from the statistical analysis after microarray quality check due to high background. Total of 7 samples.
2015-04-27 | E-GEOD-63247 | biostudies-arrayexpress
Project description:Mitochondria are subcellular organelles that are more than just the powerhouse of cells, they also dictate if a cell dies or survives. The mitochondrial outer-membrane voltage-dependent anion channel 1 (VDAC1) has been shown to play a crucial role in metabolism and apoptosis, however its involvement in ischemic pathologies and cancer is not clear. Transcriptome analysis of Vdac1-/- mouse embryonic fibroblasts (MEF) highlighted cancer and inflammation as top diesases but also activation of the HIF-1 signaling pathway in normoxia. HIF-1α protein was stable due to ROS accumulation that decreased respiration and glycolysis and maintained basal apoptosis. However, in hypoxia increased activation of ERK in combination with maintenance of respiration and increased glycolysis counterbalanced the deleterious effects of ROS, thereby allowing Vdac1-/- MEF to proliferate better than wild-type MEF. Xenografts of RAS-transformed Vdac1-/- MEF in mice showed stabilization of both HIF-1α and HIF-2α which led to blood vessel destabilization and a strong inflammatory response. Moreover, expression of Cdkn2a, a HIF-1-target and tumor suppressor gene, was strongly decreased. Consequently RAS-transformed Vdac1-/- MEF tumors grew faster than wild-type MEF tumors. These findings provide new perspectives into the understanding of VDAC1 in the function of mitochondria not only in cancer but also in inflammatory diseases.
2015-04-27 | GSE63247 | GEO
Project description:Mitochondria play a critical role in initiating and amplifying ferroptosis. VDAC1 embedded in the mitochondrial outer membrane, exerts a crucial role in regulation of ferroptosis. However, the mechanisms of VDAC1 oligomerization in regulating ferroptosis are not well elucidated. Here, we identified that VSTM2L, a novel VDAC1 binding protein, is positively associated with prostate cancer (PCa) progression, and a key regulator of ferroptosis. Moreover, VSTM2L knockdown in PCa cells enhanced the sensibility of RSL3-induced ferroptosis. Mechanistically, VSTM2L forms complex with VDAC1 and HK2, enhancing their binding affinity and preventing VDAC1 oligomerization, thereby inhibiting ferroptosis and maintaining mitochondria homeostasis in vitro and in vivo. Collectively, our findings reveal a pivotal role for VSTM2L in driving ferroptosis resistance and highlight its potential as a ferroptosis-inducing therapeutic target for the treatment of PCa.
2025-05-07 | PXD052173 | Pride
Project description:Mitochondria from affected tissues of Amyotrophic Lateral Sclerosis (ALS) patients show morphological and biochemical abnormalities. The impairment of mitochondrial functions causes oxidative damage and accumulation of ROS and represents one of the major features that lead to the selective death of motor neurons in ALS. Our aim was to assess the ability of oxidative stress found in ALS to induce post-translational modifications (PTMs) in VDAC1, the main protein of the outer mitochondrial membrane and known to interact with SOD1 mutants related to ALS. In this work, specific post-translational modifications (PTMs) of the VDAC1 protein purified by hydroxyapatite from mitochondria of a NSC34 cell line expressing human SOD1G93A, a suitable ALS motor neurons model, were analyzed by tryptic and chymotryptic proteolysis and UHPLC/High Resolution ESI-MS/MS. Selective deamidations of asparagine and glutamine of VDAC1 in ALS-related NSC34-SOD1G93A cells but not in NSC34-SOD1 or NSC34wt cells were found. In addition, we identified differences in the over-oxidation of methionine and cysteines between VDAC1 purified from ALS model or non-ALS NSC34 cells. The specific range of PTMs identified exclusively in VDAC1 from NSC34-SOD1G93A cells but not fromNSC34control lines, suggests the appearance of important changes to the structure of the VDAC1 channel and therefore to the bioenergetics metabolism of ALS motor neurons.
2020-12-10 | PXD022598 | Pride
Project description:Functions of AtVDAC1 and its partner p26 in Arabidopsis thaliana. We previously showed that knock-out mutants impaired in AtVdac1 and p26 (AtVdac1 protein partner) are hypersensitive to salicylic acid: the root growth is more inhibited in response to 30 uM salicylic acid (SA) compared to the wild type. We want to know now which genes are up- or down-regulated in the mutants in control and SA conditions.<br> We want to compare the RNAm contents in the wild type, vdac1 and p26 mutants and, vdac1-p26 double mutant. One-week old plantlets were transferred for 2 hours on a fresh medium containing either 0 or 30uM salicylic acid.<br> Arabidopsis lines (WT, vdac1.1, p26.1, vdac1.1-p26.1) were grown in vertical position on ABIS medium (Lanquar et al., 2006). One week-old seedlings were transferred on a fresh ABIS medium containing either 0 or 30 uM salicylic acid. After 2 hours, the all seedlings were harvested. Three replicates were done; total RNAs from these 3 experiments were mixed together for the transcriptomic analysis.
2007-06-19 | E-MEXP-795 | biostudies-arrayexpress