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5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (RNA-seq)

ABSTRACT: 5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (RNA-seq)

PROVIDER: PRJNA1077087 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27983158_1.fastq.gz	Fastqsanger.gz
	SRR27983158_2.fastq.gz	Fastqsanger.gz
	SRR27983159_1.fastq.gz	Fastqsanger.gz
	SRR27983159_2.fastq.gz	Fastqsanger.gz
	SRR27983160_1.fastq.gz	Fastqsanger.gz

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5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles

Project description:5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles

| PRJNA1076882 | ENA

5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (smallRNA seq)

Project description:5-Fluorouracil (5-FU) has been used for chemotherapy for colorectal and other cancers for over 50 years. The prevailing view of its mechanism of action is inhibition of thymidine synthase leading to defects in DNA replication and repair. However, 5-FU is also incorporated into RNA causing defects in RNA metabolism, inhibition of pseudouridine modification, and altered ribosome function. We examined the impact of 5-FU on the expression and export of small RNAs into small extracellular vesicles (sEVs) and regulation of post-transcriptional small RNA modifications (PTxMs). EVs are secreted by all cells and contain a variety of proteins and RNAs that can function in cell-cell communication. PTxMs on cellular and extracellular small RNAs provide yet another layer of gene regulation. We found that treatment of colorectal cancer (CRC) cells with 5-FU represses sEV export of miRNA and snRNA-derived RNAs, but promotes export of snoRNA-derived RNAs. Strikingly, 5-FU treatment significantly decreased the levels of pseudouridine on both cellular and sEV small RNA profiles. In contrast, 5-FU exposure led to increased levels of cellular small RNAs containing a variety of methyl-modified bases. Our results suggest that 5-FU exposure leads to altered expression, base modification, and mislocalization of sEV small RNAs.

2024-09-18 | GSE255876 | GEO

5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (RNA-seq)

2024-09-18 | GSE255875 | GEO

5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (smallRNA seq)

Project description:5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles (smallRNA seq)

| PRJNA1077086 | ENA

5-Fluorouracil Treatment Represses Pseudouridine-Containing miRNA Export into Extracellular Vesicles

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-09-18 | GSE255877 | GEO

FMRP facilitates the nuclear export of N6-methyladenosine-containing mRNAs

Project description:FMRP facilitates the nuclear export of N6-methyladenosine-containing mRNAs.

2019-11-21 | GSE133724 | GEO

Pseudouridine in small RNAs

Project description:Pseudouridine is an isomer of uridine and is the most common RNA modification in both procaryotes and eucaryotes. It is found in ribosomal, transfer, and other structural RNA as well as in some mRNA and non-coding RNA. We have found abundant pseudouridine in small RNA and their precursors in Arabidopsis.

2023-08-07 | GSE230228 | GEO

Pseudouridine in small RNAs

2023-08-07 | GSE222751 | GEO

Knockout of Pseudouridine synthase 1 (PUS1) in mice. [Kidney]

Project description:In an effort to produce a mouse model of Mitochondrial Myopathy with Lactic acidosis and Sideroblastic Anemia (MLASA), we knocked out the gene for Pseudouridine synthase 1 (PUS1), an enzyme that modifies uridine to pseudouridine in many cytoplasmic and mitochondrial tRNAs, as well as other cellular RNAs. The Pus1-/- mice are viable, are born at the expected Mendelian frequency, and are non-dysmorphic. The PUS1 mRNA and certain pseudouridine modifications are absent in cytoplasmic and mitochondrial tRNAs in the Pus1-/- mice. The Pus1-/- mice display reduce exercise capacity at 14 weeks, with alterations in muscle morphology, histology, and physiology. Red gastrocnemius muscle from Pus1-/- mice shows reduced number and size of mitochondria and reduced Cytochrome C oxidase activity. Two-condition, two-color experiment: Mouse wild type PUS1 and homozygous mutant PUS1 kidney tissue samples: 4 biological replicates each.

2016-05-16 | E-GEOD-77819 | biostudies-arrayexpress

Knockout of Pseudouridine synthase 1 (PUS1) in mice. [Liver]

Project description:In an effort to produce a mouse model of Mitochondrial Myopathy with Lactic acidosis and Sideroblastic Anemia (MLASA), we knocked out the gene for Pseudouridine synthase 1 (PUS1), an enzyme that modifies uridine to pseudouridine in many cytoplasmic and mitochondrial tRNAs, as well as other cellular RNAs. The Pus1-/- mice are viable, are born at the expected Mendelian frequency, and are non-dysmorphic. The PUS1 mRNA and certain pseudouridine modifications are absent in cytoplasmic and mitochondrial tRNAs in the Pus1-/- mice. The Pus1-/- mice display reduce exercise capacity at 14 weeks, with alterations in muscle morphology, histology, and physiology. Red gastrocnemius muscle from Pus1-/- mice shows reduced number and size of mitochondria and reduced Cytochrome C oxidase activity. Two-condition, two-color experiment: Mouse wild type PUS1 and homozygous mutant PUS1 liver tissue samples: 4 biological replicates each.

2016-05-16 | E-GEOD-77820 | biostudies-arrayexpress

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