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ABSTRACT: si-fto-RNA-seq in ovary

PROVIDER: PRJNA1067203 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27679234_1.fastq.gz	Fastqsanger.gz
	SRR27679234_2.fastq.gz	Fastqsanger.gz
	SRR27679235_1.fastq.gz	Fastqsanger.gz
	SRR27679235_2.fastq.gz	Fastqsanger.gz
	SRR27679236_1.fastq.gz	Fastqsanger.gz

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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

Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE24811: Time Series of Mouse skeletal muscle cell differentiation GSE24852: ChIP-Seq of MyoD, Myf5, Snai1, HDAC1, HDAC2, E47 and empty vector controls in mouse skeletal myoblasts or myotubes GSE38236: RNA-Seq of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated myoblasts Refer to individual Series

2012-07-04 | E-GEOD-24904 | biostudies-arrayexpress

RNA-seq of K562 cells treated with the FTO inhibitor CS2 compared to DMSO treated cells

Project description:Increased FTO expression has been connected to resistance to tyrosine kinase inhibitors in CML. To explore the therapeutic potential of targeting FTO in CML, we tested the FTO catalytic inhibitor in the K562 CML cell line. The RNA-seq was performed to identify relevant regulated genes.

2023-12-31 | E-MTAB-12774 | biostudies-arrayexpress

A lncRNA from the FTO locus acts as an inhibitor of the m6A writer complex and p53 tumor suppression signaling

Project description:control RNA and FTO-IT1 RNA and their interacting proteins were pulled down by biotin-streptavidin beads to see the interacting protein of FTO-IT1 RNA.

2024-08-09 | PXD041053 | Pride

Obesity-associated variants within FTO form long-range functional connections with IRX3

Project description:Genome-wide association studies in diverse populations have reproducibly associated variants within introns of FTO with increased risk for obesity and type-2 diabetes.While the molecular mechanisms linking these noncoding variants with obesity are not immediately obvious, subsequent studies in mice demonstrated that FTO expression levels influence body mass and composition phenotypes. Yet, no direct connection between the obesity-associated intronic variants and FTO expression or function has been made. We show that the obesity-associated noncoding sequences within FTO are functionally connected, at megabase distances, primarily with the homeobox gene IRX3, rather than with FTO. 4C-seq samples for Fto/fto and Irx3/irx3a genes promoters in different samples: adult mouse brain, E9.5 mouse embryos and 24hpf zebrafish embryos.

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Mus musculus

Project description:RNA-seq data of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated mouse primary myoblasts

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RNA seq with AML (NB4) cells upon FTO inhibition

Project description:To determine the potential targets of FTO and identify treatment significance of FTO inhibition in AML, we conducted transcriptome wide RNA seq with NB4 cells upon DMSO and FTO inhibitors (FB23 and FB23-2) treatment.

2019-04-29 | GSE103495 | GEO

Drosophila sp. (in: flies)

Project description:Drosophila ovary RNA-seq

| PRJNA866605 | ENA

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

2013-06-15 | E-GEOD-47216 | biostudies-arrayexpress

The m6A demethylase FTO promotes C/EBPβ-LIP translation to perform oncogenic functions in breast cancer cells (RNA-sequencing)

Project description:RNA-sequencing (RNA-seq) results of MDA-MB-231 cells; two scrambled shRNA control (SCR) replicates and two FTO knockdown (shFTO) replicates.

2025-02-21 | E-MTAB-14808 | biostudies-arrayexpress

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