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The ER stress sensor IRE1 interacts with STIM1 to promote store-operated calcium entry, T cell activation, and muscular differentiation

ABSTRACT: The ER stress sensor IRE1 interacts with STIM1 to promote store-operated calcium entry, T cell activation, and muscular differentiation

PROVIDER: PRJEB70257 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR12303890.fastq.gz	Fastqsanger.gz
	ERR12303891.fastq.gz	Fastqsanger.gz
	ERR12303892.fastq.gz	Fastqsanger.gz
	ERR12303893.fastq.gz	Fastqsanger.gz
	ERR12303894.fastq.gz	Fastqsanger.gz

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Store-operated Ca2+ entry in follicular T cells controls humoral immune responses and autoimmunity

Project description:T follicular helper (TFH) cells promote affinity maturation of B cells in germinal centers (GCs), whereas T follicular regulatory (TFR) cells limit GC reaction. Store-operated Ca2+ entry (SOCE) through Ca2+ release-activated Ca2+ (CRAC) channels mediated by STIM and ORAI proteins is a fundamental signaling pathway in T lymphocytes. Here we show that SOCE is required for the differentiation and function of both TFH and TFR cells. Conditional deletion of Stim1 and Stim2 genes in T cells or Treg cells results in spontaneous autoantibody production and humoral autoimmunity. Conversely, antibody-mediated immune responses following viral infection critically depend on SOCE in TFH cells. Mechanistically, STIM1 and STIM2 control early TFR and TFH cell differentiation through NFAT-mediated IRF4, BATF and Bcl-6 expression. SOCE plays a dual role in GC response by controlling TFH and TFR cell function, thus enabling protective B cell responses and preventing humoral autoimmunity. RNAseq analyses of WT and Stim1Stim2 DKO follicular T cells and non-follicular T cells; 4-6 mice per cohort in duplicates. Mice were infected for 10 days with LCMV.

2016-03-10 | E-GEOD-79039 | biostudies-arrayexpress

The ER stress sensor IRE1 interacts with STIM1 to promote store-operated calcium entry, T cell activation, and muscular differentiation

Project description:A quantitative phosphoproteomic study was performed on mouse embryonic fibroblasts (MEF) knocked-out of IRE1 protein and re rexpressin it culturen in 25mM glucose media. The chosen experimental strategy was to perform phosphopeptide enrichment associated with multiplex protein identification and quantification by LC-MSMS on a high-resolution mass spectrometer using tandem mass tag (TMT9; Thermo Fisher Scientific) technology and High- Select Fe-NTA Phosphopeptide Enrichment Kit (Thermo Fisher Scientific).

2023-12-08 | PXD046579 | Pride

Store-operated Ca2+ entry in follicular T cells controls humoral immune responses and autoimmunity

2016-03-10 | GSE79039 | GEO

The ER stress sensor IRE1 interacts with STIM1 to promote store-operated calcium entry, T cell activation, and muscular differentiation

Project description:CAMPARI2 CRISPR screening for SOCE modulators of ER stress. PC cells were sorted and sequenced for CRISPR whole KO library (De brie). Unsorted, SOrte din LOW PC and LOW PC Tunica treated fro 4hours were analysed.

2023-12-09 | E-MTAB-13548 | biostudies-arrayexpress

Chronic dysfunction of Store-operated calcium entry by pulsed RNAi induction in fat tissue impairs organismal energy homeostasis in Drosophila

Project description:The purpose is to have a overview on how chronic dysfunction of store-operated calcium entry change transcription profiles of adult fly fat tissue. Methods:To achieve chronic dysfunction of store-operated calcium entry, we carried out the Temperature-caused RNAi Pulse Induction of Stim (29 celcius degree incubation, Stim-TRiPI, or Stim-TRIP in data file) in fat storage tissue of 6 days old adult male flies. At day 10 and 11 after Stim-TRiPI (Stim-TRIP), we isolated the fat tissues and carried out RNAseq analysis based gene-level read counts.

2019-05-07 | GSE112689 | GEO

Differential regulation of membrane potential during store-operated calcium entry in neutrophil subsets

Project description:Calcium signals are initiated in immune cells by the process of store-operated calcium entry (SOCE), where receptor activation triggers transient calcium release from the endoplasmic reticulum, followed by opening of plasma membrane calcium-release activated calcium (CRAC) channels. ORAI1, ORAI2 and ORAI3 are known to comprise the CRAC channel, however the contributions of individual isoforms to neutrophil function is not well understood. Here we show that loss of ORAI1 partially decreases calcium influx while loss of both ORAI1 and ORAI2 completely abolishes store-operated calcium entry. In other immune cell types, loss of ORAI2 enhances SOCE. In contrast, we find that ORAI2-deficient neutrophils display decreased calcium influx, which is correlated with measurable differences in regulation of neutrophil membrane potential via KCa3.1. Decreased SOCE in ORAI1-, ORAI2- and ORAI1/2-deficient neutrophils impairs multiple neutrophil functions including phagocytosis, degranulation, leukotriene and ROS production, rendering ORAI1/2-deficient mice highly susceptible to staphylococcal infection. This study demonstrates that ORAI1 and ORAI2 are the primary components of the neutrophil CRAC channel and identifies novel subpopulations of neutrophils where cell membrane potential functions as a rheostat to modulate the SOCE response. These findings have implications for new mechanisms that modulate neutrophil function during infection, acute and chronic inflammatory conditions, and cancer.

2020-09-01 | GSE157200 | GEO

Selective modulation of gene expression in activated normal human peripheral blood mononuclear cells by store-operated calcium entry blocker BTP2

Project description:Calcium is a critical signaling molecule in many cell types including immune cells. The calcium-release activated calcium channels (CRAC) responsible for store-operated calcium entry (SOCE) in immune cells are gated by STIM family members functioning as sensors of Ca2+ store content in the endoplasmic reticulum. We investigated the effect of SOCE blocker BTP2 on human peripheral blood mononuclear cells (PBMC) stimulated with the mitogen phytohemagglutinin (PHA).

2023-08-07 | GSE226570 | GEO

Store operated Ca2+ entry (SOCE) controls ameloblast cell function and enamel development

Project description:Abstarct:Mutations in the endoplasmic reticulum (ER) Ca2+ sensor stromal interaction molecule 1 (STIM1) result is a number of disease states including abnormal enamel formation. However, these defects in enamel have remained unclear given a lack of animal models available. We generated Stim1/2K14Cre mice to ablate the activity of STIM1 and its homologue STIM2 in enamel cells. These mice showed impaired Ca2+ entry in enamel cells and although enamel formed, it was severely hypomineralized and mechanically weak. RNA-sequencing of enamel cells provided a global overview of loss of Ca2+ sensor activity. ER stress markers associated with unfolded protein response (UPR) were increased. Cell morphology was altered showing loss of the typical ruffled-border and mislocalized mitochondria. We also identified decreased glutathione system and potentially associated with this, increased ROS and abnormal mitochondria. The Ca2+ extrusion system and enamel gene expression were also altered. These data might represent the first in vivo study linking Stim1/2 ablation with increased UPR function, decreased glutathione metabolism, increased ROS and abnormal mitochondria. Loss of ER Ca2+ sensors Stim1/2 in enamel cells has substantial detrimental effects at the cell and mineral phase level.

2017-01-17 | GSE93655 | GEO

STIM1 regulates store-operated Ca2+ entry in oocytes.

Project description:The single transmembrane-spanning Ca(2+)-binding protein, STIM1, has been proposed to function as a Ca(2+) sensor that links the endoplasmic reticulum to the activation of store-operated Ca(2+) channels. In this study, the presence, subcellular localization and function of STIM1 in store-operated Ca(2+) entry in oocytes was investigated using the pig as a model. Cloning and sequence analysis revealed the presence of porcine STIM1 with a coding sequence of 2058 bp. In oocytes with full cytoplasmic Ca(2+) stores, STIM1 was localized predominantly in the inner cytoplasm as indicated by immunocytochemistry or overexpression of human STIM1 conjugated to the yellow fluorescent protein. Depletion of the Ca(2+) stores was associated with redistribution of STIM1 along the plasma membrane. Increasing STIM1 expression resulted in enhanced Ca(2+) influx after store depletion and subsequent Ca(2+) add-back; the influx was inhibited when the oocytes were pretreated with lanthanum, a specific inhibitor of store-operated Ca(2+) channels. When STIM1 expression was suppressed using siRNAs, there was no change in cytosolic free Ca(2+) levels in the store-depleted oocytes after Ca(2+) add-back. The findings suggest that in oocytes, STIM1 serves as a sensor of Ca(2+) store content that after store depletion moves to the plasma membrane to stimulate store-operated Ca(2+) entry.

| S-EPMC2693300 | biostudies-literature

Transcription profiling of human monoclonal cell lines with high or low levels of store-operated Ca2+ entry

Project description:This series of microarray experiments monitored the gene expression profiles for monoclonal cell lines (derived from HEK-293 parental cell culture) with high (H1, H15, H24, H36, H39) or low (L3, L28, L29) levels of store-operated Ca2+ entry (SOCE). For selection of clones, HEK-293 cells were loaded with indo-1 and sorted by FACS on the basis of their cyclopiazonic acid (CPA)-stimulated Ca2+ entry. Monoclonal cell lines were selected from the sorted cells and their levels of SOCE confirmed by monitoring thapsigargin-stimulated Ba2+ entry. Total RNA was extracted from cells immediately after removal from their growth environment. RNA was processed and hybridized to the Affymetrix HG-U133A chip. Two parallel hybridizations were done for each RNA preparation from each monoclonal cell line or from the parental HEK-293 cell culture.

2007-08-03 | E-GEOD-1309 | biostudies-arrayexpress

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