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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data of inducible stable cell lines overexpressing Ero1alpha WT and Ero1alpha C104A/C131A

ABSTRACT: The overall cellular response to oxidative stress generated by Ero1M-NM-1 in the lumen of the mammalian endoplasmic reticulum (ER) is poorly characterized. Here, we investigate the effects of overexpressing a hyperactive mutant (C104A/C131A) of Ero1M-NM-1. Using microarray analysis, we demonstrate that the cell reacts to the oxidative challenge caused by Ero1M-NM-1 hyperactivity by turning on the unfolded protein response. Our findings suggest that the hyperoxidation generated by Ero1M-NM-1-C104A/C131A is addressed in the ER lumen and is unlikely to exert oxidative injury throughout the cell. Human embryonic kidney 293 Flp-In T-REx cells (Invitrogen) overexpressing Ero1M-NM-1-WT and Ero1M-NM-1-C104A/C131A were grown in triplicates and expression was either not induced or induced doxycycline (dox) for 24 h. Extracted RNA was hybridized on Affymetrix microarrays and genes with significantly different expression levels between the four categories were identified by a two-way analysis of variance (ANOVA), where the cell line (Ero1M-NM-1-WT or Ero1M-NM-1-C104A/C131A) and induction status (-dox/+dox) were used as the two factors for the p-value calculation.

ORGANISM(S): Homo sapiens

SUBMITTER: Henning Gram Hansen

PROVIDER: E-GEOD-40601 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data of inducible stable cell lines overexpressing Ero1alpha WT and Ero1alpha C104A/C131A

Project description:The overall cellular response to oxidative stress generated by Ero1α in the lumen of the mammalian endoplasmic reticulum (ER) is poorly characterized. Here, we investigate the effects of overexpressing a hyperactive mutant (C104A/C131A) of Ero1α. Using microarray analysis, we demonstrate that the cell reacts to the oxidative challenge caused by Ero1α hyperactivity by turning on the unfolded protein response. Our findings suggest that the hyperoxidation generated by Ero1α-C104A/C131A is addressed in the ER lumen and is unlikely to exert oxidative injury throughout the cell.

2012-09-07 | GSE40601 | GEO

Expression status of mRNA for sex hormone receptors in human dental pulp cells and the response to sex hormones in the cells

Project description:Objectives: Sex hormone receptors are reported to be present in human dental pulp (HDP) cells. The purpose of this study was to examine the biological significance of estrogen and androgen receptors (ER and AR, respectively) in HDP cells. Design: We isolated HDP cells expressing ER- and AR-mRNAs and investigated the expression status of the receptors and the response to sex hormones in the cells. Results: HDP cells expressing ER- and/or AR-mRNAs had the ability to form alizarin red S-positive nodules in which calcium and phosphorus were deposited in vitro and to differentiate into odontoblasts-like cells and dentin-like tissue in vivo. Individual clones isolated from HDP cells exhibited a different expression pattern of mRNA for ER and AR. Some clones expressed ERM-NM-1- and/or ERM-NM-2-mRNAs and the others coexpressed ER- and AR-mRNAs. Using the Ingenuity software, we found that 17M-NM-2-estradiol (E2) and dihydrotestosterone (DHT) could act directly on HDP cells through ER- or androgen signaling-mediated mechanisms. E2 or DHT stimulated the mRNA expression for genes related to odontogenesis of dentin-containing teeth and odontoblast differentiation, suggesting that ER and AR in HDP cells may be involved in dentinogenesis. Conclusions: Our findings provide new insights into the biological significance of sex hormone receptors in HDP cells. Gene expression profiles of human dental pulp cells derived from one male patient were compared between cells treated with 10^-6 M 5alpha-dihydrotestosterone and cells treated with vehicle. Each sample has one replicate. Gene expression profiles of human dental pulp cells derived from one female patient were compared between cells treated with 10^-9 M 17beta-estradiol and cells treated with vehicle. Each sample has one replicate.

2013-03-28 | E-GEOD-44677 | biostudies-arrayexpress

Quantitative analysis of differential expressed genes and pathways in AB8 cells overexpressing Crb2 S267A variant for 48h (+dox) compared to non-induced control cells (-dox) using next-generation sequencing (NGS)

Project description:Purpose: NGS can be used for system-based analysis of cellular pathways. The goal of this study was to identify genes and pathways which are activated in AB8 podocytes due to Crb2 S267A overexpression. Methods: AB8 cells were modified using lentiviral transduction with pIND21_hCrb2+GFP_S267A. After selection with puromycin, cells were induced with doxycycline for 48h to overexpress Crb2 S267A variant. Non-induced cells were used as controls. RNA-seq data from AB8 cells overexpressing Crb2 S267A variant for 48h (+dox) were compared with non-induced control cells (-dox) (n=4). Activated pathways (GO terms) were identified with DAVID bioinformatics tool. Results: RNAseq data revealed activation of ER stress response, chaperon folding genes and pathways. Misfolded Crb2 variant induces cellular ER stress compared to control cells.

2021-04-15 | GSE148661 | GEO

The Mammalian Cytosolic Thioredoxin Reductase Pathway Acts via a Membrane Protein to Reduce ER-localised Proteins

Project description:Folding of proteins entering the mammalian secretory pathway requires the insertion of the correct disulfide bonds. Disulfide formation involves both an oxidative pathway for their insertion and a reductive pathway to remove incorrectly formed disulfides. Reduction of these disulfides is critical for correct folding and degradation of misfolded proteins. Previously, we showed that the reductive pathway is driven by NADPH generated in the cytosol. Here, by reconstituting the pathway using purified proteins and ER microsomal membranes, we demonstrate that the thioredoxin reductase system provides the minimal cytosolic components required for reducing proteins within the ER lumen. In particular, saturation of the pathway and its protease sensitivity demonstrates the requirement for a membrane protein to shuttle electrons from the cytosol to the ER lumen. These results provide compelling evidence for the critical role of the cytosol in regulating ER redox homeostasis to ensure correct protein folding and to facilitate the degradation of misfolded ER proteins.

2020-04-09 | PXD017923 | Pride

Enzyme-mediated proximity labeling identifies small RNAs in the endoplasmic reticulum lumen

Project description:In eukaryotic cells, the subcellular targeting of RNA controls many fundamental aspects of cellular physiology. RNA molecules are broadly distributed throughout the nucleoplasm and cytoplasm, but are conventionally believed to be excluded from the secretory pathway compartments, including the endoplasmic reticulum (ER). Recent discovery of RNA N-glycan modification (glycoRNAs) has challenged this view, but direct evidence of RNA localization in the ER lumen has been lacking. In this study, we applied enzyme-mediated proximity labeling to profile the ER lumen-localized RNAs in human embryonic kidney 293T cells and rat cortical neurons. Our dataset revealed the presence of small non-coding RNAs in the ER lumen, including U RNAs, sco/sca RNAs and Y RNAs, which partially overlap with glycoRNAs. These findings shed light on novel RNA targeting mechanism and raise interesting questions regarding the biological functions of ER lumenal RNAs.

2024-03-10 | GSE227266 | GEO

Differential expression of genes involved in the transtion to Doxorubicin drug resistance in MCF7 breast cancer cells

Project description:Summary: Cancer imparts an increased risk for venous thromboembolism (VTE). Direct mechanisms linking VTE with malignancy remain unknown. Our characterization of Doxorubicin (DOX)-resistant MCF7 breast cancer cells revealed links with antithrombotic pathways, as an anticoagulant transcriptional profile was observed. Specifically, the intracellular anticoagulant Tissue Factor Pathway Inhibitor 1 (TFPI1) protein was elevated and functional in all resistant models tested; TFPI1 accumulation coincided with reduced thrombin. TFPI1 overexpression in unselected cells elevated pro-malignant gene markers and increased DOX resistance. Furthermore, TFPI1 and Breast Cancer Resistant Protein (BCRP) levels increased early and remained sustained during selection. Finally, consistent with antithrombin-mediated hypoxic metastasis, Hypoxia-Inducible Factor 1 alpha (HIF1alpha) was elevated in drug resistant and TFPI1 overexpressing cells. Thus, increased TFPI1 may create an intratumoral hypoxic environment, potentially leading to drug resistance. MCF7 cells were selected for DOX resistance by first treating the cells with 1 microM DOX for 48 hours. The cells were then exposed to 100 nM DOX for 2 weeks. After this period, the surviving cells were resistant to further DOX treatment.

2013-06-01 | E-MTAB-1643 | biostudies-arrayexpress

Gene expression profiles of CARM1 overexpression in MCF7

2011-06-01 | GSE26454 | GEO

NOX4 links metabolic regulation in pancreatic cancer to endoplasmic reticulum redox vulnerability and dependence on PRDX4

Project description:PDAC cells acquire metabolic changes that augment NADPH production and cytosolic redox homeostasis. Here we show that high NADPH levels drive activity of NADPH oxidase 4 (NOX4) expressed in the endoplasmic reticulum (ER) membrane. NOX4 produces H2O2 metabolized by Peroxiredoxin 4 (PRDX4) in the ER lumen. Using functional genomics and subsequent in vitro and in vivo validations, we find that PDAC cell lines with high NADPH levels are dependent on PRDX4 for their growth and survival. PRDX4 addiction is associated with increased reactive oxygen species, a DNA-PKcs-governed DNA damage response and radiosensitivity, which can be rescued by depletion of NOX4 or NADPH. As such, this study has identified NOX4 as a protein which paradoxically converts the reducing power of the cytosol to an ER-specific oxidative stress vulnerability in PDAC that may be therapeutically exploited by targeting PRDX4.

2021-05-25 | GSE166165 | GEO

Gene expression profiles of CARM1 overexpression in MCF7

Project description:The goal of this study is to identify ERalpha-target genes affected by overexpression of the histone arginine methyltransferase CARM1 in breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 overexpressing MCF7 cell line where CARM1 is overexpressed by 2 fold to determine the created a Dox-inducible CARM1 overexpressing MCF7 cells for evaluation of the global effects of CARM1 on Eralpha-target gene expression. MCF7-tet-on-CARM1 clone 13 were treated under 4 conditions: DMSO; Dox; E2 (10nM); Dox+E2. In Dox+E2 condition, cells were pre-treated with Dox for 5 days before treating with E2 for 4 hours. 3 biological replicates were included and total of 12 samples were analyzed.

2011-06-01 | E-GEOD-26454 | biostudies-arrayexpress

Transcription profiling of mouse C2AS12 cells infected with (1) wt p300 + tTA, (2) p300deltaTAZ2 +tTA, (3) wt p300 +tTA +doxycycline to define the transcriptional network regulated by ectopic expression of the transcriptional co-activator protein, p300 and define its role in promoting muscle cell survival

Project description:The primary focus of these studies is to define the transcriptional network regulated by ectopic expression of the transcriptional co-activator protein, p300, in order to define its mechanism(s) of action in promoting muscle cell survival. Our laboratory has generated a murine C2-derived myoblast cell line stably expressing an IGF-II cDNA in antisense orientation (C2AS12 cells). These cells proliferate normally in serum-rich growth medium but progressively die in low-serum differentiation medium. Ectopic expression of p300 (a transcriptional co-coactivator with acetyltransferase activity) prevents the progressive cell death induced by serum withdrawal, however, the mechanism of this action is not understood. Further, over-expression of a mutated form of p300, lacking at protein interaction domain (deltaTAZ2), failed to maintain cell viability although it retains catalytic activity. Wild-type and mutant p300 are delivered using recombinant adenoviruses (Ad-p300 and Ad-p300deltaTAZ2) and their expression is regulated by a second recombinant adenovirus encoding the tetracycline transactivator protein (Ad-tTA), affording regulated expression of p300 forms (Tet-off system) and providing a control for viral load. Using these reagents the overall experiment was as follows: Three parallel series of C2AS12 cells were infected with (1) wt p300 + tTA, (2) p300deltaTAZ2 +tTA, (3) wt p300 +tTA +doxycycline. Infected cells were grown to confluence followed by transfer to low-serum differentiation medium (T0). Cell were isolated at this point and following 24 (T24) hours incubation for RNA isolation. Companion dishes of cells were included for analysis by immunocytochemistry to ensure regulated transgene expression and cell viabilities. 6 biological replicates, representing 3 treatment groups, two timepoints and 2 biological outcomes (cell survival with p300wt and apoptotic cell death with p300wt+Dox and p300mut)

2007-12-07 | E-GEOD-4224 | biostudies-arrayexpress

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