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

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

PROVIDER: PRJNA825555 | ENA |

REPOSITORIES: ENA

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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

Extracellular Signals Induce Dynamic ER Remodeling through TAT1-dependent Microtubule Acetylation

Project description:Dynamic changes in the endoplasmic reticulum (ER) morphology are central to maintaining cellular homeostasis. Microtubules (MT) facilitate the continuous remodeling of the ER network into sheets and tubules by coordinating with many ER-shaping protein complexes, although how this process is controlled by extracellular signals remains unknown. Here we report that TAK1, a kinase responsive to various growth factors and cytokines including TGF- and TNF-, triggers ER tubulation by activating TAT1, an MT-acetylating enzyme that enhances ER-sliding. We show that this TAK1/TAT1-dependent ER remodeling promotes cell survival by actively downregulating BOK, an ER membrane-associated proapoptotic effector. While BOK is normally protected from degradation when complexed with IP3R, it is rapidly degraded upon their dissociation during the ER sheets-to-tubules conversion. These findings demonstrate a distinct mechanism of ligand-induced ER remodeling and suggest that the TAK1/TAT1 pathway may be a key target in ER stress and dysfunction.

2024-06-16 | PXD045865 | Pride

Induction of ER stress in HCT116 colon cancer cells

2015-04-01 | GSE63252 | GEO

Transcriptomic analysis of cardiomyocyte upon OSKM induction

Project description:Transcriptomic analysis of cardiomyocyte upon OSKM induction

| PRJNA674836 | ENA

ER stress response in hepatocytes upon Plasmodium infection

Project description:Upon infection of a mammalian host, Plasmodium parasites first replicate inside hepato-cytes, generating thousands of new parasites. Although Plasmodium intra-hepatic devel-opment represents a substantial metabolic challenge to the host hepatocyte, how infected cells respond to and integrate this stress remains poorly understood. Here, we present proteomic and transcriptomic analysis revealing that the endoplasmic reticulum (ER)-resident unfolded protein response (UPR) is activated in host hepatocytes upon Plasmo-dium berghei infection. The expression of XBP1s -the active form of the UPR mediator XBP1- and the liver-specific UPR mediator CREBH is induced by P. berghei infection in vivo. Furthermore, this UPR induction increases parasite liver burden. Altogether, our data suggests that ER stress is a central feature of P. berghei intra-hepatic development, contributing to the success of infection.

2016-04-20 | PXD002269 | Pride

Induction of ER stress in HCT116 colon cancer cells

Project description:To investigate the role of p53 and DICER in the induction of ER stress, wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells were treated with the ER stress inducers tunicamycin or brefeldin A for 24 hours. Microarray analysis was used to determine changes in gene expression associated with the induction of ER stress, and to compare this induction in wildtype, p53 knockout or DICER mutant HCT116 colon cancer cells Triplicate samples of HCT116 wildtype, HCT116 p53 knockout and HCT116 DICEREX5/EX5 cells were treated with with 0.5 mg/ml of BFA or 2 mg/ml of Tm for 24 h. Following treatment, cells were harvested and lysed in TRIzol reagent and RNA was extracted. Microarray analysis was carried out using Affymetrix HG-U133_Plus-2 arrays.

2015-04-01 | E-GEOD-63252 | biostudies-arrayexpress

Campylobacter jejuni Cas9 is necessary for efficient infection of Caco-2 cells and cell stress induction

Project description:Objective: We previously showed that Campylobacter jejuni Cas9 was necessary for full virulence and efficient induction of human cell stress followed by cell death, but no virulence mechanism could be unravelled then. Therefore, we carried out global genome-wide transcriptomics, using RNA samples extracted from cells infected by a wild-type C. jejuni strain and the corresponding cas9 deletion strain. Methods: Caco-2 epithelial cells were infected with C. jejuni wild-type or cas9 deletion strains and RNA was extracted at 5 timepoints post-infection. Results: Wild-type C. jejuni induced cellular stress, DNA damage and cell death pathways in Caco-2 cells continuously from 30 min up to 4 hours after infection, eventually followed by visual cell death induction after 24 hours; the corresponding cas9 deletion strain did also induce cell stress pathways within the first two hours of infection but at later timepoints, stress pathway induction had dropped and after 4 hours of infection, expression of the corresponding stress genes had normalised to near-t=0 (uninfected) expression values; the cas9 deletion strain did not lead to visual cell death induction after 24 hours. Conclusions: Campylobacter jejuni Cas9 is necessary for full virulence of C. jejuni and is involved in the efficient induction of cellular stress pathways and eventually, cell death.

2018-09-30 | GSE89661 | GEO

Gene expression profile in Caco-2 cells upon co-treatment with lovastatin and selective AHR ligands

Project description:We report high-throughput profiling of gene expression from human colon adenocarcinoma Caco-2 line. We profile mRNA in lovastatin-treated cells, and examine the effect of AHR ligands, SGA360 or SGA315. This study provides a framework for understanding transcriptional changes caused by SGA360 or SGA315 during upon lovastatin use.

2020-04-23 | GSE130234 | GEO

Transcriptome analysis of Caco-2 Cells upon deoxynivalenol and its acetylated exposure

Project description:Transcriptome analysis of Caco-2 Cells upon deoxynivalenol and its acetylated exposure

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Mapping H3K9me3 enrichment upon heterochromatin induction in early embryos.

Project description:Mapping H3K9me3 enrichment upon heterochromatin induction in early embryos.

| PRJNA1168518 | ENA