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RNA-seq Analysis of mRNA profiles in β-Gal-overexpressing, and HuR-overexpressing primary hepatocytes

ABSTRACT: RNA-seq Analysis of mRNA profiles in β-Gal-overexpressing, and HuR-overexpressing primary hepatocytes

PROVIDER: PRJNA639611 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12019373_1.fastq.gz	Fastqsanger.gz
	SRR12019373_2.fastq.gz	Fastqsanger.gz
	SRR12019374_1.fastq.gz	Fastqsanger.gz
	SRR12019374_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA-seq Analysis of mRNA profiles in β-Gal-overexpressing, and HuR-overexpressing primary hepatocytes.

Project description:Purpose: The goal of this study is to investigate how HuR regulates hepatocyte death. Methods: mRNA profiles of β-Gal-overexpressing, and HuR-overexpressing primary hepatocytes were generated by deep sequencing using an Illumina Novaseq 6000 platform. Paired-end clean reads were aligned to the mouse reference genome(GRCm38.p6) with Hisat2 v2.0.5, and the aligned reads were used to quantify mRNA expression by using featureCounts v1.5.0-p3. Conclusion: Our study represents the detailed analysis of mRNA profiles in HuR-overexpressing primary hepatocytes, generated by RNA-seq technology. Our results show that 2677 genes were upregulated and 2712 genes were downregulated following HuR overexpression. GO analysis indicated that the upregulated genes were primarily related to inflammation response and apoptotic signaling pathway. These data indicate that upregulation of HuR in hepatocytes leads to cell death.

2023-07-08 | GSE154015 | GEO

RNA-seq Analysis of mRNA profiles in β-Gal-overexpressing, and HuR-overexpressing primary hepatocytes

Project description:Purpose: The goal of this study is to investigate how HuR regulates hepatocyte death. Methods: mRNA profiles of β-Gal-overexpressing, and HuR-overexpressing primary hepatocytes were generated by deep sequencing using an Illumina HiseqX platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.83) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of mRNA profiles in HuR-overexpressing primary hepatocytes, generated by RNA-seq technology. Our results show that 258 genes were upregulated and 357 genes were downregulated following HuR overexpression. GO analysis indicated that the upregulated genes were primarily related to cell death, death, apoptotic process, programmed cell death and intrinsic apoptotic signaling pathway. These data indicate that upregulation of HuR leads to hepatocyte death.

2023-06-15 | GSE152542 | GEO

RNA-seq Analysis of mRNA profiles in β-Gal-overexpressing, and HuR-overexpressing primary hepatocytes.

Project description:RNA-seq Analysis of mRNA profiles in β-Gal-overexpressing, and HuR-overexpressing primary hepatocytes.

| PRJNA644869 | ENA

RNA-seq Analysis of Transcriptomes in β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing αTC1-6 cells

Project description:RNA-seq Analysis of Transcriptomes in β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing αTC1-6 cells

| PRJNA448031 | ENA

RNA-seq analysis of mRNA profiles in β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing INS-1 832/13 cells

Project description:Purpose: The goal of this study is to investigate how NIK regulates islet β-cell function. Methods: mRNA profiles of β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing INS-1 832/13 cells were generated by deep sequencing using an Illumina Hiseq platform. Paired-end clean reads were aligned to the rat reference genome (ftp://ftp.ensembl.org/pub/release-90/fasta/rattus_norvegicus/dna/) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of mRNA profiles in NIK-overexpressing and NIK(KA)-overexpressing INS-1 832/13 cells, generated by RNA-seq technology. Our results show that 471 genes were upregulated and 249 genes were downregulated following NIK overexpression. GO analysis indicated that the upregulated genes were primarily related to the immune response. KEGG pathway enrichment analysis showed that immune signaling pathways, including the TNF, NF-κB, antigen processing and presentation signaling pathways, were significantly activated by NIK overexpression in INS-1 832/13 cells, whereas genes related to insulin secretion and regulation of secretion were significantly decreased. NIK(KA), the dominant-negative mutant of NIK, does not induce the expression of genes related to immune response in INS-1 832/13 cells.

2020-07-28 | GSE130121 | GEO

RNA-seq analysis of mRNA profiles in β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing INS-1 832/13 cells

Project description:RNA-seq analysis of mRNA profiles in β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing INS-1 832/13 cells

| PRJNA534032 | ENA

RNA-seq Analysis of Transcriptomes in β-Gal-overexpressing, NIK-overexpressing, and NIK(KA)-overexpressing αTC1-6 cells

Project description:Purpose: The goal of this study is to determine the molecular mechanisms involved in the NIK regulation of α cell function. Methods: mRNA profiles of β-Gal control, NIK, and NIK(KA) overexpressed αTC1-6 cells were generated by deep sequencing using an Illumina Hiseq platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.89) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of NIK-overexpressing aTC1-6 cell transcriptomes, generated by RNA-seq technology. Our results show that 328 genes were upregulated and 48 genes were downregulated following NIK overexpression. GO analysis indicated that the upregulated genes were primarily related to the immune response. KEGG pathway enrichment analysis showed that immune signaling pathways, including the TNF, NF-κB, and chemokine signaling pathways, were significantly activated by NIK overexpression in aTC1-6 cells, while genes related to metabolism-associated signal pathways were significantly decreased. NIK(KA), the dominant-negative mutant of NIK, does not affect gene expression in aTC1-6 cells.

2018-12-30 | GSE112511 | GEO

Sequencing of liver RNA from HuR WT and HuR KO mice

Project description:We aimed to identify genes that are altered upon deletion of HuR in hepatocytes under steady state conditions.

2021-09-15 | GSE143358 | GEO

Effects of genetic ablation and pharmacological inhibition of HuR on gene expression, iron metabolism and hormone levels.

Project description:BackgroundHuR/ELAV1, a ubiquitous RNA-binding protein, belongs to the RNA-binding protein family and is crucial for stabilizing and regulating the translation of various mRNA targets, influencing gene expression. Elevated HuR levels are associated with multiple disorders, including cancer and neurodegenerative diseases. Despite the identification of small molecule inhibitors targeting HuR, their detailed characterization remains limited. Recently, Eltrombopag, an FDA-approved drug for immune thrombocytopenic purpura and chemotherapy-induced thrombocytopenia, emerged as a potential HuR inhibitor. However, the specific molecular pathways influenced by both HuR and Eltrombopag are not fully understood. ResultsOur study demonstrates that Eltrombopag operates via HuR inhibition, affecting gene expression regulation at the posttranscriptional level. We show that both HuR knockout and Eltrombopag treatment modulate iron metabolism by decreasing ferritin heavy chain (FTH1) and light chain (FTL) synthesis while increasing the expression of Iron-regulatory protein 2 (IRP2), a key regulator of ferritin translation. Additionally, HuR inhibition reduces the levels of Glycoprotein Hormones, Alpha Polypeptide (CGA), a marker associated with hormone-induced tumors, suggesting a potential use of Eltrombopag in treatment of cancers overexpressing CGA. We observed that the main of control is manifested at the level of translation inhibition, with proteosome-mediated regulation also playing an important role.ConclusionsThese findings uncover novel posttranscriptional mechanisms governed by HuR and its inhibitor, elucidating pathways relevant to HuR-mediated regulation and molecular therapies aimed at targeting this protein.

2024-12-20 | PXD050698 | Pride

Intestinal epithelial HuR balances counteracting RNA networks to protect against intestinal inflammation and cancer. PART 2 Differentiality in mRNA expression between Control mice and mice overexpressing Elavl1.

Project description:Elavl1/HuR is a ubiquitous and conserved RNA-binding protein that binds to a U-rich RNA motif that shuttles between nucleus and cytoplasm. In epithelia, the elevated expression of HuR assumingly promotes degeneration and cancer suggesting that its generic suppression may provide clinical benefits. In this study we focused on biological and clinical functions of HuR in intestinal epithelial cells and we presented evidence that changes in HuR levels induce polarized distortions in these cells to support different pathologic outcomes. Here we study the differentiality in mRNA abundance between Control mice and mice overexpressing Elavl1 (TgATF-HuR). Control and TgATF-HuR mice were treated with Dimethylhydrazine (DMH)/Dextran Sodium Sulphate (DSS) for 60 days and tumors where dissected from large intestines; those with sizes between 10-15mm2 were pooled to generate samples with 4 tumors/sample and snap frozen. Three samples per genotype were used either for RIP analyses or total RNA extraction. Isolated RNA was used for microarray or qRT-PCR analyses.

2020-07-01 | E-MTAB-4017 | biostudies-arrayexpress

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