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Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation [MDA-MB-468-RNASeq]

ABSTRACT: Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation [MDA-MB-468-RNASeq]

PROVIDER: PRJNA989605 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25099145.fastq.gz	Fastqsanger.gz
	SRR25099146.fastq.gz	Fastqsanger.gz
	SRR25099147.fastq.gz	Fastqsanger.gz
	SRR25099148.fastq.gz	Fastqsanger.gz
	SRR25099149.fastq.gz	Fastqsanger.gz

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Similar Datasets

Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation [MDA-MB-468-RNASeq]

Project description:Here we show that nitric oxide (NO) is a potent inhibitor of FTO demethylase activity by directly binding to the catalytic iron center, which causes global m6A hypermethylation of mRNA in cells and results in gene-specific enrichment of m6A on mRNA of NO-regulated transcripts. Both cell culture and tumor xenograft models demonstrated that endogenous NO synthesis can regulate m6A-mRNA levels and transcriptional changes of m6A-associated genes. These results build a direct link between NO and m6A-mRNA regulation and reveal a novel signaling mechanism of NO as an endogenous regulator of the epitranscriptome.

2024-06-30 | GSE236269 | GEO

Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation

Project description:Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation

| PRJNA989601 | ENA

Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation [MDA-MB-231-meRIPSeq]

2024-06-30 | GSE236271 | GEO

Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation [MDA-MB-231-RNASeq]

2024-06-30 | GSE236270 | GEO

Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation [MDA-MB-231-RNASeq]

Project description:Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation [MDA-MB-231-RNASeq]

| PRJNA989607 | ENA

Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation [MDA-MB-231-meRIPSeq]

Project description:Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation [MDA-MB-231-meRIPSeq]

| PRJNA989609 | ENA

Nitric oxide inhibits FTO demethylase activity to regulate N<sup>6</sup>-methyladenosine mRNA methylation.

Project description:N6-methyladenosine (m6A) is the most abundant internal modification on eukaryotic mRNAs. Demethylation of m6A on mRNA is catalyzed by the enzyme fat mass and obesity-associated protein (FTO), a member of the nonheme Fe(II) and 2-oxoglutarate (2-OG)-dependent family of dioxygenases. FTO activity and m6A-mRNA are dysregulated in multiple diseases including cancers, yet endogenous signaling molecules that modulate FTO activity have not been identified. Here we show that nitric oxide (NO) is a potent inhibitor of FTO demethylase activity by directly binding to the catalytic iron center, which causes global m6A hypermethylation of mRNA in cells and results in gene-specific enrichment of m6A on mRNA of NO-regulated transcripts. Both cell culture and tumor xenograft models demonstrated that endogenous NO synthesis can regulate m6A-mRNA levels and transcriptional changes of m6A-associated genes. These results build a direct link between NO and m6A-mRNA regulation and reveal a novel signaling mechanism of NO as an endogenous regulator of the epitranscriptome.

| S-EPMC10623363 | biostudies-literature

Nitric oxide inhibits FTO demethylase activity to regulate N6-methyladenosine mRNA methylation

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

2024-06-30 | GSE236272 | GEO

FTO Regulates Activation of Rho GTPases Signaling as N6-methyladenosine RNA Demethylase and an Rhotekin Partner Protein

Project description:Reversible RNA modification of N6-methyladenosine (m6A) plays a critical role in post-transcriptional gene regulation1-13. Although the fat mass and obesity-associated protein (FTO) has been previously shown to function as an m6A demethylase in nuclear RNA1,14, its exact function in disease pathogenesis remains a mystery. Here, we demonstrate that FTO suppresses the activation of Rho GTPase signaling via both its demethylation activity and specific interaction with Rho effector, Rhotekin (RTKN)15. The knockdown of FTO activates RhoA and RhoC, induces stress fibres, and accelerates cell migration. Endogenous RTKN is highly expressed in certain cancer and cancer-derived cell lines16,17 with overexpression of RTKN leading to moderate activation of Rho18. We further found that overexpression of RTKN blocks nuclear import of FTO and traps FTO in the cytoplasm to mediate m6A demethylation of cytosolic mRNA, thereby changing gene expression by preventing m6A-dependent mRNA decay and translation. Our results illustrate how FTO represses Rho activation through m6A demethylation and direct interaction with RTKN, and shed new light on FTO-dependent post-transcriptional gene regulation in RTKN overexpressed cancers, which may provide a new direction for developing anti-cancer therapies.

2018-12-31 | GSE83540 | GEO

FTO regulates adult neurogenesis through modulating the dynamics of N6-methyladenosine

Project description:Fat mass and obesity-associated gene (FTO) is a member of the Fe (II) and oxoglutarate-dependent AlkB oxygenase family, and has been linked to obesity and intellectual disability. However, the role of FTO in neurodevelopment and neurogenesis remains largely unknown. Here, we show that FTO is expressed in adult neural stem cells (aNSCs) and neurons, and displays dynamic expression during postnatal neurodevelopment. The loss of FTO leads to the decreased brain size and body weight. We found that FTO deficiency could reduce the proliferation and neuronal differentiation of aNSCs in vivo, which leads to the impaired learning and memory. Given the role of FTO as a demethylase of N6-methyladenosine (m6A), we further performed the genome-wide m6A profiling and observed the dynamic m6A modification during postnatal neurodevelopment. The loss of FTO could lead to the altered m6A modifications on the mRNAs of several key components of BDNF pathway. These results together suggest that FTO play important roles in neurogenesis and learning and memory.

2017-04-20 | GSE94098 | GEO

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