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Expression profile of select glucose and lipid metabolic genes mediated by STIM1 knockout, or STIM1 knockout plus Snail1 overexpression in SMMC7721 cells

ABSTRACT: To investigate the altered glucose and lipid metabolism genes after STIM1 knockout (STIM1 KO) or STIM1 knockout plus Snail1 OE (STIM1 KO+Snail1 OE) in SMMC7721 cells. STIM1 KO-SMMC7721 cells were constructed by CRISPR/Cas9, and STIM1 KO+Snail1 OE-SMMC7721 cells was established via lentiviral Infection of Snail1 overexpression in STIM1 KO-SMMC7721 cells. The cells mentioned above were cultured in DMEM supplemented with 10% (v/v) FBS at 37 °C in 5% CO2. When the cells grow to 60~70% confluent, total RNA was extracted by using Trizol (TAKARA, Japan). Reverse transcription was performed from 1μg total RNA using PrimeScript™ RT reagent Kit with gDNA Eraser (TAKARA), Quantitative real-time PCR were performed (CFX386, BioRad) with 40 cycles at 95 °C for 10 seconds, 59 °C for 20 seconds and 72 °C for 30 seconds.

ORGANISM(S): Homo sapiens

PROVIDER: GSE148129 | GEO | 2020/04/07

REPOSITORIES: GEO

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Expression profile of select glucose and lipid metabolic genes mediated by STIM1-Snail1 circuit in SMMC7721 cells

Project description:To investigate the altered glucose and lipid metabolic genes after Snail1 overexpression, Snail1 plus STIM1 double overexpression in SMMC7721 cells. Snail1 overexpression (Snail1 OE)- and Snail1 plus STIM1 double overexpression(Snail1+STIM1 dOE)- SMMC7721 cells were established via lentiviral Infection. The cells mentioned above were cultured in DMEM supplemented with 10% (v/v) FBS at 37°C in 5% CO2. When the cells grow to 60~70% confluent, Total RNA was extracted by using Trizol (TAKARA, Japan). Reverse transcription was performed from 1μg total RNA using PrimeScript™ RT reagent Kit with gDNA Eraser (TAKARA), Quantitative real-time PCR were performed (CFX386, BioRad) with 40 cycles at 95 oC for 10 seconds, 59 oC for 20seconds and 72 oC for 30 seconds.

2019-08-17 | GSE135901 | GEO

Expression profile of select glucose and lipid metabolic genes mediated by STIM1 knockout in SMMC7721 cells

Project description:To investigate the altered glucose and lipid metabolic genes after STIM1 knockout in SMMC7721 cells. STIM1 knockout SMMC7721 cells were constructed by CRISPR/Cas9. The cells mentioned above were cultured in DMEM supplemented with 10% (v/v) FBS at 37°C in 5% CO2. When the cells grow to 60~70% confluent, Total RNA was extracted by using Trizol (TAKARA, Japan). Reverse transcription was performed from 1μg total RNA using PrimeScript™ RT reagent Kit with gDNA Eraser (TAKARA), Quantitative real-time PCR were performed (CFX386, BioRad) with 40 cycles at 95 °C for 10 seconds, 59 °C for 20seconds and 72°C for 30 seconds.

2019-08-17 | GSE135900 | GEO

Expression profile of select glucose and lipid metabolic genes mediated by STIM1 knockout, or STIM1 knockout plus Snail1 overexpression in SMMC7721 cells

Project description:Expression profile of select glucose and lipid metabolic genes mediated by STIM1 knockout, or STIM1 knockout plus Snail1 overexpression in SMMC7721 cells

| PRJNA623315 | ENA

STIM1 Translocation to The Nucleus Protects Cells from DNA Damage

Project description:DNA damage represents a challenge for cells as this damage must be eliminated to preserve cell viability and the transmission of genetic information. To reduce or eliminate unscheduled chemical modifications in genomic DNA, an extensive signaling network, known as the DNA damage response (DDR) pathway, ensures this repair. In this work, and by means of a proteomic analysis aimed at the study of the STIM1 protein interactome, we have found that STIM1 is closely related to the protection from endogenous DNA damage, replicative stress, as well as in the response to interstrand crosslinks (ICLs). Here we show that STIM1 has a nuclear localization signal (NLS) that mediates its translocation to the nucleus, and that this translocation and the association of STIM1 to chromatin is enhanced in response to mitomycin C (MMC), an ICL-inducing agent. Consequently, STIM1-deficient cell lines show a higher level of basal DNA damage, replicative stress, and a higher sensitivity to MMC. We show that STIM1 normalizes FANCD2 protein levels in the nucleus, explaining the increased sensitivity to MMC in STIM1-KO cells. Our results show for the first time a nuclear function for the endoplasmic reticulum protein STIM1 and increase the number of genes involved in DNA repair.

2023-12-22 | PXD041181 | Pride

Genetic changes of Hep3B cells with acquired resistance to sorafenib after STIM1 knockout

Project description:In order to explore the role of STIM1 in the acquired resistance of Hep3B cells to sorafenib, we used CRISPR Cas9 technology to knock out STIM1.

2023-12-09 | GSE248770 | GEO

Expression profile of select glucose and lipid metabolic genes mediated by STIM1-Snail1 circuit in SMMC7721 cells

Project description:Expression profile of select glucose and lipid metabolic genes mediated by STIM1-Snail1 circuit in SMMC7721 cells

| PRJNA560517 | ENA

STIM1 controls T cell mediated immune regulation and inflammation in chronic infection

Project description:Influence of STIM1 on the transcriptome of CD4+ T cell subsets STIM1 is critical for the regulation of the intracellular Ca2+ homeostasis in CD4+ T cell. Loss of function mutations in STIM1 in patients result in severe immuno deficiency and recurrent infections. Using conditional knock out mice for STIM1, we investigated the role of STIM1 in T cells during chronic infections by in-vivo and in-vitro experiments. We found that STIM1 is required for T cell-mediated immunity to chronic infection with Mycobacterium tuberculosis (Mtb) as STIM1-deficient mice succumb to infection faster than littermate controls, have increased mycobacterial burdens and severe pulmonary infiltration with myeloid and lymphoid cells .Using the Affymetrix Mouse Exon 1.0 platform, we analyzed the influence of STIM1 expression on the transcriptom of CD4+T cells in-vitro. We found that STIM1 is required for the regulation of apoptosis related genes after TCR stimulation as well as for the induction of a transcriptonal program that polarizes naive CD4+ T cells into inducible CD4+ T regulatory cells (iTreg). Together with our in-vivo findings, these experiments reveal that STIM1 is essential for immune regulation to prevent an injurious inflammatory response during chronic infection.

2015-03-17 | GSE66933 | GEO

STIM1-mediated gene expression in non-pathogenic and pathogenic CD4+ Th17 cells

Project description:Immunity to fungal infections is mediated by cells of the innate and adaptive immune system. Activation of immune cells requires Ca2+ influx through the Ca2+ channel ORAI1, which is activated by stromal interaction molecule 1 (STIM1). Th17 cells are essential for immunity to C. albicans infection and require Ca2+ influx for expression of IL-17A and other Th17 cytokines. In mice, deletion of STIM1 and thus Ca2+ influx in all immune cells enhanced susceptibility to mucosal C. albicans infection, whereas T cell-specific deletion of STIM1 impaired immunity to systemic C. albicans infection. STIM1 deletion in CD4 T cells had different effects on gene expression programs in pathogenic (proinflammatory) and non-pathogenic Th17 cells. STIM1 deletion in non-pathogenic Th17 cells, which are required for antifungal immunity, compromised the expression of genes in several metabolic pathways including Foxo and HIF-1a signaling as well as the TCA cycle and oxidative phosphorylation (OXPHOS). Consequently, STIM1 deficient non-pathogenic Th17 cells had impaired glycolysis and mitochondrial respiration. By contrast, STIM1 deletion in pathogenic Th17 cells showed only attenuated mitochondrial function but normal glycolysis.

2020-06-01 | GSE149162 | GEO

Transcriptome Stim1 R304W skeletal muscle

Project description:Comparative RNAseq of tibilias anterior from Stim1 R304W and WT male mice at 4 months

2021-07-07 | GSE179460 | GEO

STIM1 Mediates Calcium-dependent Epigenetic Reprogramming in Pancreatic Cancer [mRNAseq_PDX]

Project description:We characterized Gemcitabine resistant pancreatic cancer tumors and show that the co-amplification of RRM1 and STIM1 confers novel and independent properties to gemcitabine resistant cells. The upregulation of RRM1 drives gemcitabine resistance, while the amplification of STIM1 leads to increased cytosolic calcium upon stress, eliciting ER stress resistance and NFAT activation.

2021-01-14 | GSE154909 | GEO

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