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Effect of endoplasmic reticulum stress on gene expression in lymphoblastoid cell lines.

ABSTRACT: The ER stress inducing agent Thapsigargin (TG) and/or the cytoprotective agent Salubrinal were applied to lymphoblastoid cell lines. TG induced lytic replication as well as a distinct pattern of gene expression changes. This study was designed to identify host genes mediating lytic replication secondary to ER stress. DMSO or TG applied for 6 hrs then washed out, immediately followed by either (i) DMSO, or (ii) SAL resulting in 4 conditions (DMSO, TG, SAL, or TG+SAL). Total RNA harvested at 3, 24 or 72hrs for Affymetrix analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Adam Rosendorff

PROVIDER: E-GEOD-31447 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Endoplasmic reticulum stress causes EBV lytic replication.

Taylor Gwen Marie GM Raghuwanshi Sandeep K SK Rowe David T DT Wadowsky Robert M RM Rosendorff Adam A

Blood 20110817 20

Endoplasmic reticulum (ER) stress triggers a homeostatic cellular response in mammalian cells to ensure efficient folding, sorting, and processing of client proteins. In lytic-permissive lymphoblastoid cell lines (LCLs), pulse exposure to the chemical ER-stress inducer thapsigargin (TG) followed by recovery resulted in the activation of the EBV immediate-early (BRLF1, BZLF1), early (BMRF1), and late (gp350) genes, gp350 surface expression, and virus release. The protein phosphatase 1 a (PP1a)-sp ...[more]

PMID: 21849482

Similar Datasets

Effect of endoplasmic reticulum stress on gene expression in lymphoblastoid cell lines.

Project description:The ER stress inducing agent Thapsigargin (TG) and/or the cytoprotective agent Salubrinal were applied to lymphoblastoid cell lines. TG induced lytic replication as well as a distinct pattern of gene expression changes. This study was designed to identify host genes mediating lytic replication secondary to ER stress.

2011-08-23 | GSE31447 | GEO

Perturbation of placental endocrine function by endoplasmic reticulum stress leads to maladaptation of maternal hepatic glucose metabolism

Project description:To investigate whether ER stress underpins the secretion of mis-glycosylated glycoproteins by trophoblast, we treated trophoblast-like BeWo cells with the ER stress inducer thapsigargin (Tg), an inhibitor specific for sarco/endoplasmic reticulum Ca2+-ATPase.

2022-12-04 | E-MTAB-10943 | biostudies-arrayexpress

Pharmacological induction of selective endoplasmic reticulum retention as a novel strategy for cancer therapy

Project description:We analysed the difference in the surface proteome of human cells that were either subjected to ER stress (induced by thapsigargin (Tg)) only or were additionally treated with a pharmacological inhibitor against the eIF2α kinase PERK, which is localized in the endoplasmic reticulum. Compared to single ER stress, several important plasma-membrane associated kinases, showed a significant downregulation under PERK inhibition.

2020-03-02 | PXD014709 | Pride

Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR)

Project description:We are currently studying how these information-carrying oligosaccharides are involved in cellular stress responses, particularly in human genetic diseases called Congenital Disorders Of Glycosylation in which oligosaccharide assembly is defective. We are interested in endoplasmic stress responses/unfolded protein responses. ER glycans and ER lectins are intimately involved in the folding of ER proteins. Therefore, ER lectins and ER glycosyltransferases may be controlled by these stress responses, to produce and/or recognize key glycans in the stress response. Our model system is the human dermal fibroblast. We have successfully calibrated the ER stress responses in these cells by determining the magnitudes of various stress effects (such as chaperone transcription) with different forms of ER stress. We are also completing a study in which activation the signaling molecules Ire1 and ATF6 are also calibrated. We prepared multiple identical aliquots of RNA from cells stressed under several of these calibrated conditions. Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR): Study of the role of ER stress in the expression of genes for ER transferases and lectins that participate in ER folding and quality control using human skin fibroblasts. The UPR response in these cells has been calibrated using various readouts in response to different stresses: 1) 40 nM L-azetidine-2-carboxylate (AZC) 1 hour, 2) 0.2 mg/ml castanospermine, 24 hours, 3) 2 mM Dithiothreitol (DTT), 20 minutes, 4) 100nm Thapsigargin (TG), 30 minutes, 5) 5 ug/ml tunicamycin, 5 hours, 6) untreated control cells

2011-02-17 | E-GEOD-27349 | biostudies-arrayexpress

Real-time quantitative PCR analysis of human EBV-B cells during UPR

Project description:Human B cells were isolated from peripheral blood from one healthy donor and two patients with Common Variable Immunodeficiency (CVID) and were immortalized by infection with Epstein Barr virus (EBV) in vitro. Immortalized EBV-B cells (in biological triplicates) were treated twelve different ways for 4 hours: 1.untreated control, 2. Thapsigargin (Tg) 1 µM, 3. Tunicamycin (Tm) 10 µg/ml, 4. 4-phenylbutyrate (4-PBA) 1 mM, 5. Tg 1 µM plus 4-PBA 1 mM, 6. Tm 10 µg/ml plus 4-PBA 1 mM, 7. Dimethyl sulfoxide (DMSO) 1 mM, 8. Tg 1 µM plus DMSO 1 mM, 9. Tm 10 µg/ml plus DMSO 1 mM, 10. Tauroursodeoxycholic acid (TUDCA) 5 mM, 11. Tg 1 µM plus TUDCA 5 mM, and 12. Tm 10 µg/ml plus TUDCA 5 mM. We used Applied Biosystems TaqMan OpenArray Real-Time PCR System (Thermo Scientific) to quantitate gene expression of relevant genes from the cells (in technical triplicates).

2020-01-19 | GSE126201 | GEO

Transcriptional profile analysis of Caco-2 cell line upon inflammatory signals and ER stress induction

Project description:We stimulated Caco-2 cells, with the TLR5 agonist flagellin (Fl), with the chemical ER stress inducer thapsigargin (TG), or a combination of both (TGFl). This strategy mimics a pro-inflammatory response in the presence of ER stress.

2022-04-16 | GSE200626 | GEO

Inhibiting coronavirus replication by chemical ER stress, including SARS-CoV-2 and MERS-CoV

Project description:Coronaviruses (CoVs) are important human pathogens for which no specific treatment is available. Here, we provide evidence that pharmacological reprogramming of ER stress pathways can be exploited to suppress CoV replication. We found that the ER stress inducer thapsigargin efficiently inhibits coronavirus (HCoV-229E, MERS-CoV, SARS-CoV-2) replication in different cell types, (partially) restores the virus-induced translational shut-down, and counteracts the CoV-mediated downregulation of IRE1α and the ER chaperone BiP. Proteome-wide data sets revealed specific pathways, protein networks and components that likely mediate the thapsigargin-induced antiviral state, including HERPUD1, an essential factor of ER quality control, and ER-associated protein degradation complexes. The data show that thapsigargin hits a central mechanism required for CoV replication, suggesting that thapsigargin (or derivatives thereof) may be developed into broad-spectrum anti-CoV drugs.

2021-06-24 | PXD021222 | Pride

Signal Transducer and Activator of Transcription 3 limits Epstein-Barr virus lytic-activation in B lymphocytes.

Project description:We used microarrays to identify genes differentially expressed in EBV-infected human B cells supporting lytic replication vs. those refractory to EBV lytic replication. We used serum from EBV-positive subject (compared to serum from EBV-negative subject) to FACS-separate lytic and refractory cells following treatment of HH514-16 cells with NaB, a lytic cycle inducing agent. RNA from sorted-lytic and sorted-refractory cells were hybridized to microarray.

2013-08-21 | E-GEOD-49568 | biostudies-arrayexpress

PERK signaling through C/EBPδ contributes to ER stress-induced expression of immunomodulatory and tumor promoting chemokines by cancer cells.

Project description:Expression of the transcription factor CEBPD is induced at early stages of the endoplasmic reticulum (ER) stress response. In order to identify the genes modulated by CEBPD during the ER stress response, we transiently silenced CEBPD expression in MDA-MB-435 melanoma cells and isolated mRNA at 6 h of treatment with Thapsigargin or DMSO control. As control, cells were transfected with two different control siRNA oligonucleotides. Results provide insights into which genes are modulated by CEBPD and/or Thapsigargin in MDA-MB-435 cell

2021-11-01 | GSE131048 | GEO

Up-regulation of ATF4-LAMP3 axis by ORF45 facilitate lytic replication of Kaposi’s sarcoma-associated herpesvirus

Project description:To investigate the regulation of ER stress-related gene expression by KSHV-ORF45 during lytic replication, we performed RNA-sequencing analysis of iSLK-BAC16 vs. iSLK-STOP45 cells under lytic induction for 72h. When the differentially expressed genes were filtered and analyzed, we found that ER stress-related gene expression was much low in iSLK-STOP45 cells compared with iSLK-BAC16 cells, indicating that ORF45 expression is required for induction of ER stress.To further reveal the signal transduction of LAMP3 in KSHV lytic replication, RNA-sequencing analysis was performed to identify the differentially expressed genes (DEGs) in normal vs. LAMP3-silenced cells under lytic replication. A total of 35372 raw read targets were obtained and all DEG clusters were filtered and analyzed by KEGG pathway enrichment analysis. Eleven pathway were significantly enriched over 10 fold in LAMP3-depleted cells compared with control cells, including PI3K-Akt signaling pathway.Given that Akt and ERK activation play the important roles in KSHV lytic replication, we conclude that LAMP3 might promote Akt and ERK activation and then consequently facilitate KSHV lytic replication.

2022-11-09 | GSE192724 | GEO

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