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RIP-seq of Ythdf3 in MEFs with or without nutrient starvation

ABSTRACT: RIP-seq of Ythdf3 in MEFs with or without nutrient starvation

PROVIDER: PRJNA666149 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12730381_1.fastq.gz	Fastqsanger.gz
	SRR12730381_2.fastq.gz	Fastqsanger.gz
	SRR12730382_1.fastq.gz	Fastqsanger.gz
	SRR12730382_2.fastq.gz	Fastqsanger.gz
	SRR12730383_1.fastq.gz	Fastqsanger.gz

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RIP-seq of Ythdf3 in MEFs with or without nutrient starvation

Project description:The variation of mRNA targets of mouse YTH N6-methyladenosine RNA binding protein 3 (Ythdf3) during nutrient starvation was determined by RNA immunoprecipitation and sequencing (RIP-seq).

2021-12-30 | GSE158660 | GEO

MeRIP-seq of mRNAs in MEFs with or without nutrient starvation

Project description:To investigate the dynamic m6A modification during starvation-induced autophagy, we performed MeRIP-seq in MEFs with or without nutrient deprivation and identified the variations of m6A modification on mRNAs. Briefly, the total polyadenylated mRNAs in MEFs cultured with or without nutrient-deprived medium for 2 hours were isolated using RNAiso plus reagent (Takara) followed Dynabeads mRNA Purification Kit (Invitrogen). The m6A RNA immunoprecipitation was performed using GenSeq m6A RNA IP Kit. NEBNext Ultra II Directional RNA Library Prep Kit (NEB) was used for library generation. Each experiment was conducted in two biological replicates. Methylated sites on peaks were identified by MACS2 peak-calling software (Zhang et al., 2008). Differentially methylated sites were identified by diffReps (Shen et al., 2013) with default setting.

2021-12-30 | GSE158268 | GEO

MeRIP-seq of mRNAs in MEFs with or without nutrient starvation

Project description:MeRIP-seq of mRNAs in MEFs with or without nutrient starvation

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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

Label-free quantitative proteomics for screening dynamic autophagy-related proteins during nutrient deprivation in MEFs

Project description:A Label-free quantitative proteomic profiling was performed on MEFs with or without nutrient starvation.

2022-10-15 | PXD025450 |

UASB anammox nutrient starvation

Project description:UASB anammox nutrient starvation Metagenome

| PRJNA715587 | ENA

Mus musculus strain:C57BL/6

Project description:RIP-seq of Ythdf3 in MEFs upon nutrient deprivation

| PRJNA659929 | ENA

Lysosomal fractions from MEFs under amino acid starvation and restimulation

Project description:Magnetically enriched lysosomal fractions from MEFs were prepared from cells in three different conditions: full media (control), 1 h amino acid starvation and 30 min amino acid restimulation.

2022-08-20 | PXD030172 | Pride

N6-Methyladenosine Reader YTHDF3-Mediated CEBPA Translation Maintains Genomic Stability and Stem Cells Function to Prevent Liver Injury and Hepatocellular Carcinoma [RIP-seq]

Project description:BACKGROUND & AIMS: Hepatocellular carcinoma (HCC) induced by chronic liver damage is a major cause of cancer mortality, but its precise epigenetic mechanisms are severely under studied. In addition, the role of N6-methyladenine (m6A) reader YTHDF3 in human diseases remains poorly understood. METHODS: Liver injury and hepatocarcinogenesis in mice were induced by chemical. CRISPR/Cas9 technology was used to construct Ythdf3 and Mettl14 knockout mice. Hepatic cell population characteristics was determined by means of 10X single-cell RNA-seq and flow cytometry. Cell proliferation and DNA damage were evaluated by immunofluorescence, immunohistochemistry, and western blot. Liver organoids were cultured to examine liver stem cells function. MeRIP-seq was used to reveal alterations in m6A methylation patterns impacted by chemical-induced liver injury. RIP-seq and Ribo-seq were applied to identify YTHDF3 targets and determine translation efficiency. Small interfering RNAs and dCas13b-FTO-sgRNA plasmids were used to evaluate the function of YTHDF3 and CEBPA in vitro. RESULTS: YTHDF3 depletion exacerbated chemical-induced liver injury with a reduction in functional hepatocytes and stem cells. Furthermore, METTL14 and YTHDF3-dependent RNA m6A dysregulation induced DNA damage and promoted development of HCC. Mechanistically, knockout of Ythdf3 impeded the translation of CCAAT/enhancer-binding protein-alpha (CEBPA), subsequently inhibited expression of PARP1 and PRDX2 to promote DNA damage and induce genomic instability, finally leading to liver injury and HCC. CONCLUSIONS: m6A/YTHDF3/CEBPA regulatory axis plays an essential role in governing cell fates and genomic stability, thereby preventing liver injury and HCC, and offers potential therapeutic avenue for targeting YTHDF3 and CEBPA in the treatment of HCC.

2024-02-29 | GSE259225 | GEO

Ribosome profiling of Mycobacterium tuberculosis under nutrient starvation

Project description:We have performed parallel ribosome profiling and RNA sequencing to determine which mRNAs are being translated during exponential growth and following 24 hours of nutrient starvation in the human pathogen Mycobacterium tuberculosis.

2021-02-02 | E-MTAB-8835 | biostudies-arrayexpress

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