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Homo sapiens

ABSTRACT: FTO demethyltion of N6-methyladenosine depends on the RRACH motif [m6A-seq]

PROVIDER: PRJNA396015 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5875431.fastq.gz	Fastqsanger.gz
	SRR5875431_1.fastq.gz	Fastqsanger.gz
	SRR5875431_2.fastq.gz	Fastqsanger.gz
	SRR5875432.fastq.gz	Fastqsanger.gz
	SRR5875432_1.fastq.gz	Fastqsanger.gz

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Homo sapiens

Project description:FTO demethyltion of N6-methyladenosine depends on the RRACH motif [CLIP-seq]

| PRJNA396014 | ENA

FTO demethyltion of N6-methyladenosine depends on the RRACH motif

Project description:FTO demethyltion of N6-methyladenosine depends on the RRACH motif

| PRJNA396010 | ENA

YTHDF3 improves translation initiation of mRNAs with N6-methyladenosine methylation at 5’ untranslated region by facilitating eIF2AK2 recruitment in oxaliplatin-resistant colorectal cancer - RIP-seq dataset

Project description:Oxaliplatin as a first-line drug frequently causes the chemo-resistance on colorectal cancer (CRC). N6-methyladenosine (m6A) methylation has been largely acknowledged in multiple biological functions. However, the molecular mechanisms underlying the m6A methylation in modulating anticancer drug resistance in CRC are still obscure. In present study, RIP-seq was conducted to investigate the occupancy of N6-methyladenosine RNA binding protein 3 (YTHDF3) served as “readers” that can recognize m6A modification site in HCT116 cells with oxaliplatin resistance (HCT116R). Then, YTHDF3 was knockdown by siRNA in HCT116 cells with oxaliplatin resistance, and RIP-seq was further conducted to investigate m6A methylation of HCT116, HCT116R and HCT116R cells with YTHDF3 knockdown.

2022-02-04 | E-MTAB-11321 | biostudies-arrayexpress

FTO demethyltion of N6-methyladenosine depends on the RRACH motif [m6A-seq]

Project description:The fat mass and obesity-associated (FTO) protein is a well-characterized demethylase that removes N6-methyladenosine (m6A) from animal mRNAs. However, it is unclear yet how the demethylation operates in living cells. In this study, we applied genome-wide approaches to study how FTO finds its demethylation targets in human cells. We overexpressed FTO in human HeLa cells, demonstrating that FTO effectively removes m6A from the RRACH motif enriched in the 3’UTR regions and leaves m6A at other motifs unaffected. RRACH elements are clearly enriched at FTO binding sites; however, m6A has a lower tendency to be removed from the FTO-bound RRACH. Taken together with the experimental validaton results, we propose a model in which FTO effectivly recognizes m6A-containing RRACH motifs in RNAs, leading to a faster demethylation and dissociation kinetic than the association, and consequently undectable FTO-mRNA association. However, when FTO binds to the non-m6A RRACH motif, the binding has a lower dissociation kinetics, yielding the detectable FTO binding signals which would enable FTO to have roles in regulating other mRNA processing events.

2020-03-22 | GSE101954 | GEO

FTO demethyltion of N6-methyladenosine depends on the RRACH motif [CLIP-seq]

2020-03-22 | GSE101953 | GEO

FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification [MeRIP-seq]

Project description:Cardiac fibrosis is common in cardiovascular diseases. N6-methyladenosine (m6A) is one of the most common modifications in eukaryotic mRNAs. Previous research has suggested that m6A modification is vital in cardiovascular diseases. The underlying targets of FTO were selected through transcriptome sequencing (RNA-seq) combined with methylated RNA immunoprecipitation sequencing (MeRIP-seq). According to MeRIP-seq and RNA-seq, FTO inhibited collagen synthesis in CFs.

2024-03-03 | GSE259328 | GEO

FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification

2024-03-01 | GSE257546 | GEO

VHL acts as an adaptor to promote the phosphorylation of FTO by CK2 to suppress clear cell renal cell carcinoma

Project description:Inactivation of the von Hippel-Lindau (VHL) E3 ubiquitin ligase protein is a hallmark feature of ccRCC, a clear cell renal cell carcinoma. However, elucidating how VHL loss drives ccRCC pathogenesis remains challenging. As the most abundant posttranscriptional modification of mRNA in eukaryotes, N6-methyladenine (m6A) is involved in the posttranscriptional regulation of mRNA molecules and has been found to play an important role in the biological process of tumorigenesis and cancer progression. Here, we show that VHL has a protein interaction with the m6A demethylase FTO, but does not perform the classical function of targeting FTO for ubiquitination degradation. Rather, VHL acts as an adapter that promotes CK2 phosphorylation of FTO, thereby regulating the enzymatic activity of FTO. MeRIP-Seq and RNA-seq sequencing analyses identified EGR1 as one of the FTO targets for VHL-deficient ccRCC cell survival. Mechanistically, FTO in ccRCC decreases the m6A level of EGR1 and inhibits EGR1 and P53 protein levels, thereby promoting ccRCC proliferation. In summary, our study identified FTO as a potential non-hypoxia inducible factor (HIF) classical substrate of VHL, highlighted the critical role of FTO in regulating m6A levels in ccRCC progression, and identified the CK2-FTO-EGR1-P53 regulatory axis as a potential target for the treatment of VHL-deficient ccRCC.

2025-08-08 | PXD053566 | Pride

Knock down of FTO in cervical cancer cells

Project description:FTO, an N6-methyladenosine (m6A) demethylase, can promote cervical cancer cell proliferation and migration. RNA-sequencing of SiHa cells with FTO knockdown was conducted to dissect the differentially expressed genes and the potential mechanism of FTO in cervical cancer.

2020-02-13 | GSE133517 | GEO

Analysis of N6-methyladenosine methylome (m6A) enrichment level in adipose stem and progenitor cells with or without FTO inhibition

Project description:To investigate the function of N6-methyladenosine methylome (m6A) in adipose stem and progenitor cells isolated from facial infiltrating lipomatosis (FIL-ASPCs), we analyzed m6A enrichment level in FIL-ASPCs with or without FTO inhibitor (FTO-IN-1) treatment through methylated RNA immunoprecipitation (MeRIP) sequencing.

2025-08-08 | GSE291128 | GEO

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