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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-seq2]

ABSTRACT: Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-seq2]

PROVIDER: PRJNA768332 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16183319_1.fastq.gz	Fastqsanger.gz
	SRR16183319_2.fastq.gz	Fastqsanger.gz
	SRR16183320_1.fastq.gz	Fastqsanger.gz
	SRR16183320_2.fastq.gz	Fastqsanger.gz
	SRR16183321_1.fastq.gz	Fastqsanger.gz

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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-seq2]

Project description:Improvements in living standards have led to non-alcoholic fatty liver disease (NAFLD), one of the most common chronic liver diseases worldwide. Recent studies have shown that N6-methyladenosine (m6A), a type of RNA modification, is strongly associated with many important biological processes. However, the relationship between m6A methylation modifications and NAFLD remains poorly understood. In the present study, through methylated RNA immunoprecipitation sequencing and RNA transcriptome sequencing in high fructose diet-induced NAFLD mice, we found that hypermethylation-encoding genes were mainly enriched in lipid metabolism processes. We identified 266 overlapping and differentially expressed genes (DEGs) that changed at both the mRNA expression level and m6A modification level. Among them, 193 genes displayed increased expression and m6A modification, indicating that m6A RNA modifications tend to be positively correlated with NAFLD. We further compared the high fructose diet-induced NAFLD mouse model with leptin receptor-deficient mice and found that DEGs enriched in the lipid metabolism pathway were up-regulated in both groups. In contrast, DEGs associated with the immune inflammatory response were up-regulated in the high fructose diet group, but down-regulated in leptin receptor-deficient mice. Taken together, our results demonstrate that m6A methylation modifications may play an important role in the development of NAFLD.

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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-Seq]

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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [MeRIP-Seq]

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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease

Project description:Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease

| PRJNA768331 | ENA

Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-Seq]

Project description:Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [RNA-Seq]

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Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [MeRIP-Seq]

Project description:Analysis of N6-methyladenosine Methylation Modification in Fructose-induced Non-alcoholic Fatty Liver Disease [MeRIP-Seq]

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N6-Methyladenosine methylation profile in rat H9C2 cardiomyocytes under the hypoxic stress

Project description:Hypoxia as a crucial pathogenesis factor usually results in huge harmful effects on cardiac injury and dysfunction. In our previous study (PMID: 33294289), We observe a series of differential expressed genes between transcription and translation, which may be attributed to the hypoxia-specific binding affinity of Nuclear cap-binding subunit 3 (NCBP3) at 5’ un-translation region of target genes. But the underlying molecular mechanism of NCBP3 for gene translation modulation remains unclear. Here, we conducted RIP-seq of N6-Methyladenosine methylation in H9C2 cells with the conditions of normoxic, hypoxic and with additional NCBP3 knockdown.

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Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down

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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.

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Analysis of N6-Methyladenosine Methylation Modification in Fructose-Induced Non-Alcoholic Fatty Liver Disease.

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