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TUT1 promotes PDAC progression through Alternative Splicing [3‘-seq]

ABSTRACT: TUT1 promotes PDAC progression through Alternative Splicing [3‘-seq]

PROVIDER: PRJNA875680 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21387342.fastq.gz	Fastqsanger.gz
	SRR21387343.fastq.gz	Fastqsanger.gz
	SRR21387344.fastq.gz	Fastqsanger.gz
	SRR21387345.fastq.gz	Fastqsanger.gz

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TUT1 promotes PDAC progression through Alternative Splicing [3‘-seq]

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a malignant cancer with high lethality rate. In this study, we identify that terminal Uridylyl Transferase 1 (TUT1), a specific terminal uridylyltransferase for U6 snRNA, is required for survival of PDAC, but not for that of normal adult pancreas. Mechanistically, TUT1 uridylylation activity promotes tri-snRNP assembly though facilitating the binding of LSM protein to U6 snRNA. TUT1 deletion leads to global alternative splicing (AS) changes which in turn triggers PDAC cell cycle dysregulation. Here, we reveal a novel function of TUT1 in regulating AS by modulating tri-snRNP levels and identify TUT1 as a potential therapeutic target for the treatment of PDAC.

2025-01-11 | GSE212513 | GEO

TUT1 promotes PDAC progression through Alternative Splicing [RNA-seq]

2025-01-11 | GSE212514 | GEO

TUT1 promotes PDAC progression through Alternative Splicing [RNA-seq]

Project description:TUT1 promotes PDAC progression through Alternative Splicing [RNA-seq]

| PRJNA875880 | ENA

Gene expression and alternative splicing in pancreatic ductal adenocarcinoma (PDAC) [exon level]

Project description:Alternative splicing is a key event to human transcriptome and proteome diversity and complexity. Recent evidence suggests that pancreatic cancer might possess particular patterns of splice variation that influence the function of individual genes contributing to tumour progression in this disease. The identification of new pancreatic cancer-associated splice variants would offer opportunities for novel diagnostics and potentially also represent novel therapeutic targets. In this dataset, we investigated the alterations in the splicing machinery in pancreatic adenocarcinoma (PDAC) specimens with full clinicopathological details, in comparisons to adjacent pancreatic tissues and normal tissues from donors.

2017-06-12 | GSE63111 | GEO

Gene expression and alternative splicing in pancreatic ductal adenocarcinoma (PDAC) [gene level]

2014-11-10 | GSE56560 | GEO

Gene expression and alternative splicing in pancreatic ductal adenocarcinoma (PDAC)

Project description:Gene expression and alternative splicing in pancreatic ductal adenocarcinoma (PDAC)

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Splicing factor SRSF1 promotes breast cancer progression via regulating alternative splicing

Project description:Splicing factor SRSF1 promotes breast cancer progression via regulating alternative splicing

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TUT1-catalyzed U6 snRNA 3′-end maturation is required for mRNA splicing to maintain stem cell pools during embryogenesis [RNA-Seq]

Project description:The post-transcriptional maturation of U6 snRNA 3′-end is important for spliceosomal assembly and RNA splicing, and is catalyzed by sequential enzymatic activities of TUT1 and USB1, that is, an oligo(U) tail is first added by TUT1 to the freshly transcribed U6 snRNA, and then trimmed by USB1 to generate mature U6 snRNA. However, biallelic inactivation of TUT1 or USB1 is linked to distinct human developmental disorders, and their physiological functions remain unknown. Here, using multiple genetically engineered mouse models, we show that Tut1, but unexpectedly not Usb1, is essential for the maintenance of the epiblast and neural stem cells in vivo. Loss of Tut1 weakens the interactions between essential splicing factors and U6 snRNA, causes defective RNA splicing, and triggers massive DNA damage and subsequent cell death. Importantly, cell death can be prevented by recombinant U6 snRNA containing an oligo(U) tail. These results challenge the current model of U6 snRNA 3′-end maturation and function. We propose that TUT1 is an essential U6 snRNA 3′-end maturation or repair factor, and discuss the implications of these results for understanding the etiologies of TUT1- and USB1-related human disorders.

2026-06-03 | GSE305663 | GEO

TUT1-catalyzed U6 snRNA 3′-end maturation is required for mRNA splicing to maintain stem cell pools during embryogenesis [Nanopore long-read RNA-seq]

2026-06-03 | GSE305664 | GEO

Genome wide screening for alternative splicing events in pancreatic cancer

Project description:We used Affymetrix GeneChipM-BM-. Human Exon 1.0 ST Arrays to identify alternative splicing events in 15 samples of PDAC compared to 6 non-tumor samples. Several commercial and open source software approaches for the analysis of differential splicing were tested and a subset of overlapping results was validated using RT-PCR and sequencing. Splicing variants could be validated in several genes closely related to cancer. Pathway analysis of genes predicted to be alternatively spliced revealed an enrichment of genes in categories closely related to cell-cell interactions and kinase activity. 15 samples of pancreatic ductal adenocarcinoma and 6 non tumor pancreatic samples were analyzed for alternative splicing events

2013-08-01 | E-GEOD-23397 | biostudies-arrayexpress

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