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Tristetraprolin specifically regulates the expression and alternative splicing of immune response genes in Hela cells

ABSTRACT: Tristetraprolin specifically regulates the expression and alternative splicing of immune response genes in Hela cells

PROVIDER: PRJNA470575 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7137085_1.fastq.gz	Fastqsanger.gz
	SRR7137085_2.fastq.gz	Fastqsanger.gz
	SRR7137086_1.fastq.gz	Fastqsanger.gz
	SRR7137086_2.fastq.gz	Fastqsanger.gz
	SRR7137087_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Tristetraprolin specifically binds to intron regions and regulates alternative splicing of immune response genes in HeLa cells

Project description:Tristetraprolin (TTP) regulates inflammatory and immune responses by destabilizing target mRNAs via binding to their 3’-UTR AREs. However, we first found that TTP can regulate gene expression and alternative splicing of inflammatory and immune responses genes in the absence of stimulation. In order to find the regulatory mechanisms, we performed iRIP-seq experiments in HeLa cells. iRIP-seq study revealed that TTP binding sites are enriched in the CDS and intronic RNA regions. We also found that the TTP-targets genes were enriched in positive regulation of I-kappaB kinase/NF-kappaB cascade and positive regulation of NF-kappaB transcription factor activity pathway, such as STAT4, EGR3, RELB, TRIM22, RNF25, and TRAF1. Furthermore, we found that alternative splicing of the innate immune response genes were globally regulated by TTP in HeLa cells. Genome-wide mapping of TTP-RNA interactions now reveal that dominant TTP binding near a competing constitutive splice site, whereas prevalent binding close to an alternative site often causes intron retention. This positional effect was further demonstrated by disrupting a TTP-binding site on minigene constructs and detecting their AS events. These findings suggest a mechanism for TTP to modulate splice site competition to produce opposite functional consequences in HeLa cells.

2020-03-12 | GSE130053 | GEO

Tristetraprolin specifically binds to intron regions and regulates alternative splicing of immune response genes in HeLa cells

Project description:Tristetraprolin specifically binds to intron regions and regulates alternative splicing of immune response genes in HeLa cells

| PRJNA533642 | ENA

Tristetraprolin specifically regulates the expression and alternative splicing of immune response genes in Hela cells

Project description:we cloned and overexpressed human TTP-encoding gene ZFP36 in HeLa cell in the absence of inflammatory stimuli. The transcriptomes of the control and ZFP36-overexpression cells were sequenced and subjected to analysis and validation. Upon ZFP36 overexpression, expression of genes in innate immunity, including those in type I interferon signaling pathway and viral response, were specifically up-regulated, implying a transcriptional regulatory mechanism associated with the predicted DNA binding activity of TTP. TTP preferentially regulates the alternative splicing of genes involved in positive regulation of I-B/NF-B cascade and TRIF-dependent toll-like receptor signaling pathway, MAPK signaling pathway, TNF signaling pathway and T cell receptor signaling pathways.Our study indicates that TTP may regulates immune response via alternative splicing regulation and possibly by transcriptional regulation as well, which greatly expands the current understanding of the central role of TTP in regulating immune response and tumorigenesis.

2019-03-24 | GSE114216 | GEO

Identification of RBM39-dependent alternative splicing events in HeLa cells

Project description:We report a comprehensive analysis of alterations in gene expression and alternative splicing upon RBM39 depletion and rescue in HeLa cells.

2023-06-19 | GSE202134 | GEO

Tristetraprolin specifically regulates the expression and alternative splicing of immune response genes in HeLa cells.

Project description:BackgroundTristetraprolin (TTP) is an RNA binding protein that plays a critical role in regulating proinflammatory immune responses by destabilizing target mRNAs via binding to their AU-rich elements (AREs) in the 3'-UTRs of mRNAs. A recent CLIP-seq study revealed that TTP-binding sites are enriched in the intronic regions of RNA. TTP is also a nuclear protein that exhibits putative DNA-binding activity. These features suggested that TTP might regulate gene transcription and/or alternative splicing of pre-mRNAs in the absence of stimulation.ResultsTo elucidate the regulatory pattern of TTP, we cloned and overexpressed the human TTP-encoding gene, ZFP36, in HeLa cells in the absence of inflammatory stimuli. The transcriptomes of the control and ZFP36-overexpressing cells were sequenced and subjected to analysis and validation. Upon ZFP36 overexpression, the expression of genes associated with innate immunity, including those in the type I interferon signaling pathway and viral response, were specifically upregulated, implying a transcriptional regulatory mechanism associated with the predicted DNA binding activity of TTP. TTP preferentially regulated the alternative splicing of genes involved in the positive regulation of the I-κB/NF-κB cascade and the TRIF-dependent toll-like receptor, MAPK, TNF, and T cell receptor signaling pathways.ConclusionsOur findings indicated that TTP may regulate the immune response via the regulation of alternative splicing and potentially transcription, which greatly expands the current understanding of the mechanisms of TTP-mediated gene regulation.

| S-EPMC6498542 | biostudies-literature

RBM6 promotes tumor cell apoptosis and disrupts the alternative splicing of related genes in HeLa cells

Project description:RNA binding proteins have important functions in tumorigenesis; therefore, their regulatory mechanisms should be further explored. The present study aimed to determine the regulatory roles of RNA binding motif protein 6 (RBM6) in transcription and alternative splicing in Hela cells. RBM6 expression levels and its effect on the prognosis of different tumors in The Cancer Genome Atlas database were analyzed using TIMER2.0. Short hairpin RNA was used to ablate RBM6 expression in HeLa cells. Differentially expressed genes and alternative splicing events in Hela cells were assessed using RNA sequencing and quantitative real-time reverse transcription polymerase chain reaction. RBM6 was identified as a prognostic marker for bladder urothelial carcinoma, kidney renal clear cell carcinoma, mesothelioma, and pancreatic adenocarcinoma. Knockdown of RBM6 promoted cell proliferation. In Hela cells, RMB6 regulated the expression and alternative splicing of many genes involved in tumorigenesis_x001E_related pathways, including ‘apoptotic process’, ‘mitotic cell cycle’, and ‘RNA splicing’. RBM6-regulated alternatively spliced genes (DIABLO (Diablo IAP-binding mitochondrial protein), PAK4 (P21 (RAC1) activated kinase 4) and ERCC2 (ERCC excision repair 2, TFIIH core complex helicase subunit)) were subjected to quantitative real-time reverse transcription polymerase chain reaction validation, which demonstrated the same expression trends as the RNA sequencing results. Our findings showed that RBM6 affects tumorigenesis and cancer progression by disrupting alternative splicing in HeLa cells.

2023-10-17 | GSE196600 | GEO

Identification of RBM39-dependent alternative splicing events in HeLa cells

Project description:Identification of RBM39-dependent alternative splicing events in HeLa cells

| PRJNA834774 | ENA

Alternative splicing signatures in apoptosis related genes of human HeLa cells with RNAi targeting p68 RNA helicase-DDX5

Project description:Alternative splicing profiling of apopotosis related genes in human HeLa cells (cervical cancer cell line) transfected with a plasmid expressing shRNAs targetting p68 helicase (DDX5, DEAD (Asp-Glu-Ala-Asp) box polypeptide 5) cloned into the pSuper expression vector compared to empty vector. Keywords: treated vs. untreated comparison; alternative splicing

2011-01-21 | GSE20010 | GEO

Genomewide analysis of U1C-dependent alternative splicing

Project description:To investigate whether U1C plays a role in splicing regulation in human system, we performed siRNA-mediated knockdown of U1C in HeLa cells and analyzed alternative splicing patterns by high-throughput RNA sequencing (RNAseq) RNAseq performed with poly(A)+ selected total RNA from U1C-knockdown and control-treated HeLa cells

2013-09-30 | E-GEOD-42485 | biostudies-arrayexpress

Effect of CLK2 overexpression on alternative splicing

Project description:To investigate the function CLK2 in the regulation of alternative splicing, we established HeLa cells overexpressing GFP, CLK2 (WT), or (T343A). We then performed alternative splicing analysis using data obtained from RNA-seq of the three cell lines.

2023-11-09 | GSE227673 | GEO

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