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Ca2+ release-activated Ca2+ entry is a potent host innate immune defence against influenza A virus

ABSTRACT: Ca2+ release-activated Ca2+ entry is a potent host innate immune defence against influenza A virus

PROVIDER: PRJNA494313 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7948450_1.fastq.gz	Fastqsanger.gz
	SRR7948450_2.fastq.gz	Fastqsanger.gz
	SRR7948451_1.fastq.gz	Fastqsanger.gz
	SRR7948451_2.fastq.gz	Fastqsanger.gz
	SRR7948452_1.fastq.gz	Fastqsanger.gz

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Ca2+ release-activated Ca2+ entry is a potent host innate immune defence against influenza A virus

Project description:Gene expression was determined for normal human bronchial epithelial (NHBE) cells incubated with DMSO or TG immediately prior to infection with USSR H1N1 virus for 12 hours. All of the NHBE cell stocks were obtained from QIAGEN.

2020-10-02 | GSE120730 | GEO

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

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

2016-03-10 | GSE79039 | GEO

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

Hi-C during mitotic release and G1 entry

Project description:Hi-C during mitotic release and G1 entry

| PRJNA551502 | ENA

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

Store Independent Ca2+ Entry Regulates the DNA Damage Response Pathway in Breast Cancer Cells

Project description:The mainstay of treatment for hormone responsive breast tumors is chemotherapy, followed by targeted endocrine therapy. The vast majority (80%) of estrogen receptor positive tumors also express wild type p53 protein that is the main determinant of the DNA damage response. Tumors that are ER+ and p53WT respond poorly to chemotherapy, although the underlying mechanisms are not completely understood. We describe a novel link between store independent Ca2+ entry (SICE) and resistance to DNA damaging drugs, mediated by the secretory pathway Ca2+-ATPase, SPCA2. In luminal ER+/PR+ breast cancer subtypes, SPCA2 levels are high and correlate with poor survival prognosis. Independent of ion pump activity, SPCA2 elevates baseline Ca2+ levels through SICE and drives cell proliferation. Attenuation of SPCA2 led to increased mitochondrial ROS production, DNA damage and activation of the ATM/ATR-p53 axis leading to G0/G1 phase cell cycle arrest and apoptosis. Resistance to DNA damaging agents including doxorubicin, carboplatin, and ionizing radiation could be reversed by downregulation of SPCA2 expression using curcumin. In conclusion, elevated SPCA2 drives pro-survival and chemotherapy resistance in ER+ p53WT breast tumors by suppressing the DNA damage response. Attenuation of SPCA2 expression by curcumin may have therapeutic potential in treating receptor positive breast cancer. The goal of this study is to investigate store Independent Ca2+ entry regulation of the DNA Damage Response pathway in breast cancer cells

2022-01-26 | GSE148537 | GEO

Gene expession profiles for monoclonal cell lines with high or low levels of store-operated Ca2+ entry.

2004-06-08 | GSE1309 | GEO

TCAF1 Promotes TRPV2-mediated Ca2+ Release in Response to Cytosolic DNA to Protect Stressed Replication Forks

Project description:The protection of the replication fork structure under stress conditions is essential for genome maintenance and cancer prevention. A key signaling pathway for fork protection involves TRPV2-mediated Ca2+ release from the ER, which is triggered after the generation of cytosolic DNA and the activation of cGAS/STING. The resulting CaMKK2/AMPK activation and subsequent Exo1 phosphorylation prevent aberrant fork processing, thereby ensuring genome stability. However, it remains poorly understood how the TRPV2 channel is activated by the presence of cytosolic DNA. Here we show that the TRPM8 channel-associated factor 1 (TCAF1) plays a key role in promoting TRPV2-mediated Ca2+ release under replication stress or other conditions that activate cGAS/STING. Mechanistically, TCAF1 promotes Ca2+ release by facilitating the dissociation of STING from TRPV2, thereby relieving TRPV2 repression. Consistent with this function, TCAF1 is required for fork protection, chromosomal stability and cell survival after replication stress.

2024-04-24 | GSE244205 | GEO

OCaR1, a gatekeeper of lysosomal and granular Ca2+ release and regulated exocytosis

Project description:OCaR1, a gatekeeper of lysosomal and granular Ca2+ release and regulated exocytosis

| PRJNA434189 | ENA