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M6A-RIP-seq of heat shock-exposed HeLa cells upon HSATIII knockdown

ABSTRACT: m6A-RIP-seq of heat shock-exposed HeLa cells upon HSATIII knockdown

PROVIDER: PRJNA689542 | ENA |

REPOSITORIES: ENA

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m6A-RIP-seq of heat shock-exposed HeLa cells upon HSATIII knockdown

Project description:To investigate the effect of HSATIII lncRNA on m6A modification, we performed m6A-RIP(RNA immuno precipitation) RNA-seq from heat shock-exposed HeLa cells upon HSATIII knockdown.

2021-04-30 | GSE164200 | GEO

m6A-RIP-seq of mRNA in HeLa cells undergoing EMT

Project description:We report the application of m6A-RIP-seq to indentify the m6A modifications variation in genes invovled in EMT. Briefly, total polyadenylated RNA was isolated from HeLa cells treated with or without 10 ng/ml TGF-β for 3 days by use of TRIZOL reagent followed the using of FastTrack MAGMaxi mRNA isolation kit (Invitrogen). RNA fragmentation, m6A-seq, and library preparation were performed according to instructions of manufacture and the previously published protocol (Wang et al., 2015). NEBNext Ultra Directional RNA Library Prep Kit (New England BioLabs, Ipswich, MA) was used for library preparation. Each experiment was conducted in two biological replicates. m6A-seq data were analyzed according to the protocols described before (Wang et al., 2015). Significant peaks with FDR < 0.05 were annotated to RefSeq database (hg19). Sequence motifs were identified by using Homer. Gene expression was calculated by Cufflinks using the sequencing reads from input samples. Cuffdiff was used to find the DE genes.

2019-03-25 | GSE112795 | GEO

m6A-RIP-seq of Ascl1-induced neurons.

Project description:We performed m6A-RIPs in Ascl1-induced neurons (iNeurons) to investigate the neuronal m6A epitranscriptome. Immunoprecipitation was done twice using two different antibodies, acquired from Abcam and Synaptic Systems (SySy), allowing for a more robust detection of m6A modification marks. Additionally, RIP-seq was performed separately with intact and fragmented RNA. The former approach allowed to identify proportions of m6A-modified transcripts among the total number, while the latter approach provided the information to identify genomic coordinates of m6A peaks.

2023-07-12 | E-MTAB-9542 | biostudies-arrayexpress

m6A-RIP-seq of mRNA in HeLa cells undergoing EMT

Project description:m6A-RIP-seq of mRNA in HeLa cells undergoing EMT

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LEAD-m6A-seq data of HeLa mRNA

Project description:We applied LEAD-m6A-seq to 11 sites of HeLa mRNA to probe m6A modification at the target sites.

2020-11-01 | GSE158389 | GEO

Mettl3-mediated m6A modification controls postnatal liver development by modulating Hnf4a-centred regulatory network [m6A-RIP-RNA-seq]

Project description:m6A-RIP sequencing of mouse liver tissues at different time points after birth.

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The m6A methyltransferase Mettl3 deficiency attenuates hepatic stellate cell activation and liver fibrosis [m6A-RIP-seq]

Project description:m6A-RIP sequencing of primary hepatic stellate cells (HSCs) isolated from Control and HSC-specific Mettl3-knockout (Mettl3 cKO) mouse liver tissues.

2022-07-13 | GSE207908 | GEO

The m6A reader YTHDF1 attenuates fulminant hepatitis via MFG-E8 translation in an m6A dependent manner [RIP-seq]

Project description:We report the application of RNA-Seq, m6A-Seq and RIP-Seq to find out YTHDF1 regulate the target genes.

2023-08-21 | GSE228280 | GEO

RIP: miR-202 mimic-transfected HeLa cells vs. negative control

Project description:Potential miR-202 targets were identified using a targetome-wide RIP-based microarray. HeLa cells were transfected with either a miR-202 mimic or a scrambled single-stranded RNA negative control. RNA was isolated from total cell lysate prior to IP and from antibody-immobilized Protein G agarose beads-RNP complexes (post-IP).

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Identification of m6A-modified YTHDF2 targets by high-throughput m6A-seq and RIP-seq in HBV-infected HepG2 cells [RIP-seq]

Project description:We investigated the role of O-GlcNAcylation of m6A reader YTHDF2 in HBV-related hepatocarcinogenesis and progression. We found that YTHDF2 O-GlcNAcylation was elevated upon HBV infection through upregulated HBP. OGT-mediated YTHDF2 O-GlcNAcylation at Ser263 enhanced its protein stability, and subsequently changed the gene expression profiles. Mechanistically, we identified YTHDF2 stabilized minichromosome maintenance protein 2 (MCM2) and MCM5 mRNAs in an m6A dependent manner by high-throughput profiling of m6A-seq and RIP-seq, thereby promoting HBV-related HCC tumorigenesis. Importantly, our study proposed that targeting OGT-mediated YTHDF2 O-GlcNAcylation may be a novel strategy for potential treatment of HBV-associated liver cancer.

2023-02-15 | GSE200259 | GEO

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