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Expression data from TCF19 knockdown in HepG2 cells maintained under high glucose (40mM) condition

ABSTRACT: Expression data from TCF19 knockdown in HepG2 cells maintained under high glucose (40mM) condition

PROVIDER: PRJNA420196 | ENA |

REPOSITORIES: ENA

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Expression data from TCF19 knockdown in HepG2 cells maintained under high glucose (40mM) condition

Project description:Changes in concentration of glucose in the cellular environment results in a variety of changes in the transcription program. Liver is the primary organ for metabolic regulation in the body, and hence, any surge in circulating blood glucose leads to changes in transcriptional states of important enzymes tasked to maintain metabolic homeostasis. Chromatin modification reader proteins play an important role in maintaining metabolic homeostasis by identification of the histone modification, and facilitating recruitment of chromatin remodelling enzymes. We knocked down an important reader domain containing protein, TCF19, in human hepatocellular carcinoma cells ( HepG2) maintained under high glucose condition and used microarray to investigate the changes in gene expression profile.

2018-02-13 | GSE107471 | GEO

Chromatin Immunoprecipitation(ChIP)-seq of TCF19 in endometrial cancer cells

Project description:In our study, TCF19 was found to be upregulated in microsatellite instability (MSI) endometrial cancer and was associated with poor prognosis and immune exhaustion signature. Elevated TCF19 enhanced cell proliferation and migration, which promoted tumorigenicity under non-immunological background; Moreover, tumoral TCF19 expression could also promote CD8+T cell exhaustion in tumor immune microenvironment, which facilitated immune escape and tumor development. Therefore, TCF19 could be a promising biomarker and effective therapeutic target for MSI endometrial cancer.

2023-08-11 | GSE218096 | GEO

RNA sequencing of TCF19 knockdown by siRNA in endometrial cancer cells

2023-08-11 | GSE218098 | GEO

Genome-wide analysis of normal and high glucose condition

Project description:Transcriptional profiling of Mouse cavernous primary pericytes (MCPs) in comparing normal glucose condition with high glucose condition

2021-01-21 | GSE146357 | GEO

Effects of glucose exposures on gene expressions in HepG2 cells

Project description:SULT1E1, the enzyme that specifically and effectively sulfates estrogens to its inactive forms-sulfated estrogens has been found to be highly induced in high glucose (450 mg/dL) cultured human liver hepatocellular carcinoma HepG2 cells. To confirm the SULT1E1 transcription in response to glucose exposures and to investigate whether glucose signal may alter the other xenobiotic metabolizing enzyme transcripts in HepG2 cells, we have conducted whole genome microarray expression profiling as a platform to identify genes that may response to glucose exposures. HepG2 cells were exposed to low glucose (40 mg/dL) or high glucose (450 mg/dL) DMEM for 48 hours respectively. The xenobiotic metabolic enzyme transcripts such as SULTs, CYPs, UGTs and GSTs were significantly altered in response to glucose exposures.

2020-08-26 | GSE140867 | GEO

Genome-wide analysis of normal and high glucose condition

Project description:Genome-wide analysis of normal and high glucose condition

| PRJNA610247 | ENA

ChIP-seq analysis of LSD2/DNA interaction in HepG2 cells in normal condition

Project description:ChIP-seq analysis of HepG2 cells revealed that many of the target genes of LSD2 were related to lipid metabolism. We found that LSD2 is an important epigenetic regulator of hepatic lipid metabolism. Examination of LSD2/DNA interaction in HepG2 cells in normal condition.

2015-02-02 | E-GEOD-59694 | biostudies-arrayexpress

TCF19 drives a broad transcriptional program that potentiates optimal innate and adaptive functions of antiviral NK cells

Project description:Natural killer (NK) cells are innate lymphocytes that play a critical role in host defense against viral infection. In addition to rapid effector cytokine production and direct cytotoxicity, NK cells exhibit features of adaptive immunity, including the capacity to undergo robust antigen-specific clonal proliferation and to generate immunological memory. However, the transcriptional programs and regulators governing dynamic NK cell responses to viral infection have not been fully uncovered. In this study, we identified Transcription factor 19 (TCF19) as a key driver of NK cell proliferation and calcium signaling in the context of mouse cytomegalovirus infection. Ablation of TCF19 was detrimental to NK cell clonal expansion and host protection against viral infection. Tcf19-/- NK cells were also unable to properly mobilize calcium downstream of antigen signaling to mediate cytotoxicity. Altogether, we find that TCF19 drives a transcriptional program that coordinates the innate and adaptive NK cell responses against viral infection.

2025-06-23 | GSE281121 | GEO

TCF19 drives a broad transcriptional program that potentiates optimal innate and adaptive functions of antiviral NK cells

2025-06-23 | GSE265814 | GEO

Transcriptional profiling of mouse cavenous endothelial cells in normal and high glucose condition

Project description:Purpose: To investigate the potential target genes associated with diabetic condition in mouse cavernous endothelial cells (MCECs) for diabetic induced erectile dysfunction (ED) treatment. Materials and Methods: Mouse cavernous tissue was embedded into Matrigel and sprouted cells were subcultivated for other studies. To mimic diabetic condition, the MCECs were exposed to normal-glucose (NG, 5 mmoL) and high-glucose (HG, 30 mmoL) condition for 72 hours. RNA-sequencing assay was performed to evaluate gene expression profiling and RT-PCR was used for sequencing data validation.

2020-09-01 | GSE146078 | GEO

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