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FTO-mediated RNA m6A demethylation regulates aggressive behavior and inflammation of fibroblast-like synoviocytes

ABSTRACT: FTO-mediated RNA m6A demethylation regulates aggressive behavior and inflammation of fibroblast-like synoviocytes

PROVIDER: PRJNA1007578 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25706700_1.fastq.gz	Fastqsanger.gz
	SRR25706700_2.fastq.gz	Fastqsanger.gz
	SRR25706701_1.fastq.gz	Fastqsanger.gz
	SRR25706701_2.fastq.gz	Fastqsanger.gz
	SRR25706702_1.fastq.gz	Fastqsanger.gz

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Transcriptome profile of fibroblast-like synoviocytes with FTO knockdown

Project description:Fibroblast-like synoviocytes (FLS) are crucial in promoting articular inﬂammation and destruction in rheumatoid arthritis (RA). As the most abundant RNA modification, the function of m6A in RA FLS is still unclear. Here, we constructed FTO-knockdown FLS to explore the mechanism of FTO in regulating the aggressive behavior of RA FLS.

2024-12-31 | GSE241249 | GEO

m6A modification profiles in RA FLS with FTO knockdown

Project description:Fibroblast-like synoviocytes (FLS) harbour active migration, invasion, proliferation and decreased cell-contact inhibition, and served as a crucial component in pathogenesis of rheumatoid arthritis. However, the mechanism underlying the aggressive behavior remain unclear. In this study, we established FTO-knockdown RA FLS to investigate the molecular mechanism.

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FTO-mediated RNA m6A demethylation regulates aggressive behavior and inflammation of fibroblast-like synoviocytes

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

2024-12-31 | GSE241254 | GEO

FTO mediates LINE1 m6A demethylation and chromatin regulation in mESCs and mouse development

Project description:N6-methyladenosine (m6A) is the most abundant internal modification on mammalian messenger RNA (mRNA). It is installed by a writer complex and can be reversed by erasers such as the fat mass and obesity-associated protein (FTO). Despite extensive research, the primary physiological substrates of FTO in mammalian tissues and development remain elusive. Here, we show that FTO mediates m6A demethylation of long-interspersed element-1 (LINE1) RNA in mouse embryonic stem cells (mESCs), regulating LINE1 RNA abundance and the local chromatin state, which in turn modulates transcription of LINE1-containing genes. FTO-mediated LINE1 RNA m6A demethylation also plays regulatory roles in shaping chromatin state and gene expression during mouse oocyte and embryonic development. Our results suggest broad effects of LINE1 RNA m6A demethylation by FTO in mammals.

2022-05-05 | GSE151780 | GEO

Differential m6A, m6Am, and m1A Demethylation Mediated by FTO in Cell Nucleus and Cytoplasm

Project description:FTO, the first RNA demethylase discovered, mediates the demethylation of N6-methyladenosine (m6A), installed internally on messenger RNA, and N6,2′-O-dimethyladenosine (m6Am), occurring at the +1 position from the 5’ cap. Despite extensive recent research on FTO, its physiological impact on cellular processes has yet to be fully elucidated. Here, we demonstrate that the cellular distribution of FTO is distinct among different cell lines, which critically affects the access of FTO to different RNA substrates. FTO binds multiple RNA substrates, including mRNA, U6 RNA, and tRNA. It mainly targets internal m6A when located in the cell nucleus and preferentially demethylates m6Am when residing in the cytoplasm. The expression levels of transcripts containing internal m6A are associated with the alteration of the FTO more so than transcripts containing m6Am. We also discover that N1-methyladenosine (m1A) in tRNA is a main substrate of FTO, with the FTO-catalyzed demethylation of target tRNAs repressing protein synthesis. Collectively, FTO-mediated RNA demethylation affects both mRNA level and translation through distinct pathways.

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SFPQ is a FTO binding protein that assists specific m6A demethylation

Project description:We identified the major RNA binding protein-SFPQ as a direct interaction partner of FTO. Our study showed that FTO and SFPQ were located in close proximity throughout the transcriptome and overexpression of SFPQ led to the demethylation of adjacent N6-methyladenosine on RNA

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Transcriptome profile of fibroblast-like synoviocytes with FTO knockdown

Project description:Transcriptome profile of fibroblast-like synoviocytes with FTO knockdown

| PRJNA1007586 | ENA

FTO mediates LINE1 m6A demethylation and chromatin regulation in mESCs and mouse tissues

Project description:N6-methyladenosine (m6A) is the most abundant internal modification in mammalian messenger RNA (mRNA). It is installed by writer proteins and can be reversed by erasers. FTO was the first RNA demethylase shown to catalyze oxidative demethylation of m6A in RNA. Despite extensive studies, the main physiological substrates of FTO and the related functional pathways remain elusive in many systems, in particular during early mammalian development. Here, we show that FTO mediates the m6A demethylation of chromosome-associated repeat RNAs in mouse embryonic stem cells (mESCs), especially the long-interspersed element-1 family (LINE1) RNA, thereby affecting their abundances to regulate chromatin state.

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Project description:Single nucleotide polymorphisms in the FTO gene encoding a m6A demthylase are associated with obesity and cancer development. However, the functional role of FTO in the developemnt of progression of hepatocellular carcinoma (HCC) as a proteotypic obesity-associated cancer remains unclear. Here, we have generated mice with hepatic FTO deficiency (FTOL-KO) and subjected them to DEN induced HCC-development. FTOL-KO mice exhibit increased HCC burden. While control mice exhibit a dynamic regulation of FTO upon induction of liver damage, this response is abrogated in mice lacking FTO. Proteomic analyses revealed that liver damage-induced increases in FTO expression promotes m6A-demethylation of CUL4A reducing its protein expression. Functionally, knockdown of CUL4A restores the increased hepatocyte proliferation observed upon loss of FTO. Collectively, our study reveals a protective role for FTO-dependent dynamic m6A mRNA demethylation of CUL4A in the initiation of HCC development.

2020-11-03 | PXD018223 | Pride

The Obesity-associated Fto gene regulates activity of the dopaminergic midbrain circuitry [FTO KO]

Project description:Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission. Profiling of m6A in midbrain and striatum from FTO knockout mice

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