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Profile of N6-methyladenosine of Pb-exposed neurons presents epitranscriptomic alterations in Pi3K-AKT pathway-associated genes

ABSTRACT: Profile of N6-methyladenosine of Pb-exposed neurons presents epitranscriptomic alterations in Pi3K-AKT pathway-associated genes

PROVIDER: PRJNA976922 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24752669_1.fastq.gz	Fastqsanger.gz
	SRR24752669_2.fastq.gz	Fastqsanger.gz
	SRR24752670_1.fastq.gz	Fastqsanger.gz
	SRR24752670_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Profile of N6-methyladenosine of Pb-exposed neurons presents epitranscriptomic alterations in Pi3K-AKT pathway-associated genes

Project description:Lead (Pb) is a pervasive heavy metal with multi-organ toxicity. However, the molecular mechanisms of Pb-induced neurotoxicity are not fully understood. The dynamics of N6-methylademine (m6A) is an emerging regulatory mechanism for gene expression, which is closely related to nervous system diseases. To elucidate the association between m6A modification and Pb-mediated neurotoxicity, primary hippocampal neurons exposed to 5 μM Pb for 48 h were used as the paradigm neurotoxic model in this study. According to the results, Pb exposure reprogrammed the transcription spectrum. Simultaneously, Pb exposure remodeled the transcriptome-wide distribution of m6A while disrupting the overall level of m6A in cellular transcripts. United analysis of MeRIP-Seq and RNA-Seq was applied to further identify the core genes whose expression levels are regulated by m6A in the process of lead-induced nerve injury. GO and KEGG analysis unveiled that the modified transcripts were overrepresented by the PI3K-AKT pathway. Mechanically, we elucidated the regulatory role of the methyltransferase like3 (METTL3) in the process of lead-induced neurotoxicity and the downregulation of the PI3K-AKT pathway. In conclusion, our novel findings shed new light on the functional roles of m6A modification in the expressional alternations of downstream transcripts caused by lead, providing an innovative molecular basis to explain Pb neurotoxicity.

2024-06-07 | GSE233621 | GEO

The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma

Project description:The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma

| PRJNA1098849 | ENA

Targeted Quantitative Profiling of Epitranscriptomic Reader, Writer and Eraser Proteins Revealed Potential Crosstalk between N6-Methyladenosine and Other RNA Modifications

Project description:N⁶-methyladenosine (m6A) and its reader, writer, and eraser (RWE) proteins assume crucial roles in regulating the splicing, stability, and translation of mRNA. To our knowledge, no systematic investigations have been conducted about the crosstalk between m6A and other modified nucleosides in RNA. Herein, we modified our recently established liquid chromatography-parallel-reaction monitoring (LC-PRM) method by incorporating stable isotope-labeled (SIL) peptides as internal or surrogate standards for profiling epitranscriptomic RWE proteins. We were able to detect reproducibly a total of 114 RWE proteins in HEK293T cells with the genes encoding m6A eraser proteins (i.e., ALKBH5, FTO) and the catalytic subunit of the major m6A writer complex (i.e., METTL3) being individually ablated. Notably, eight proteins were altered by more than 1.5-fold in the opposite directions in HEK293T cells depleted of METTL3 and ALKBH5. Analysis of published m6A mapping results revealed the presence of m6A in the corresponding mRNAs of four of these proteins. Together, we integrated SIL peptides into our LC-PRM method for quantifying epitranscriptomic RWE proteins, and our work revealed potential crosstalks between m6A and other epitranscriptomic modifications. Our modified LC-PRM method with the use of SIL peptides should be applicable for high-throughput profiling of epitranscriptomic RWE proteins in other cell types and in tissues.

2022-09-24 | PXD036032 | Pride

The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma [RNA-seq]

Project description:The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma [RNA-seq]

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The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma [RIP-seq]

Project description:The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma [RIP-seq]

| PRJNA1098859 | ENA

N6-methyladenosine circRNA Epitranscriptomic Microarray of human nucleus pulposus in intervertebral disc degeneration

Project description:N6-methyladenosine circRNA Epitranscriptomic Microarray of human nucleus pulposus in intervertebral disc degeneration

| PRJNA822413 | ENA

The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma [RNA-seq]

Project description:N6-methyladenosine (m6A) modification plays a central role in both RNA and tumor biology. Yet comprehensive m6A epitranscriptome profiling of primary tumors remains uncharted. To fill this gap, we profiled the m6A epitranscriptome of 10 non-neoplastic lung (NL) tissues and 51 lung adenocarcinoma (LUAD) tumors, integrating them with corresponding transcriptome, proteome and extensive clinical annotation. A total of 8,030 genes are marked with m6A modification, with variable abundances across tumors. Distinct clusters and genes were found to be linked exclusively to disease progression through m6A, rather than mRNA or protein levels. In comparison with NL tissues, 430 transcripts were hypo-methylated in tumors, and 222 were hyper-methylated. Fully 69% of these had no influence on RNA abundances. Amongst these genes, EML4 emerged as a novel metastatic driver, displaying significant hyper-methylation in tumors. m6A modification promoted EML4 translation and led to widespread EML4 overexpression in primary tumors. Functionally, EML4 modulated cytoskeleton dynamics and cell morphology, triggering cellular protrusions and enhancing cellular motility, local invasion, and metastasis. Clinically, high EML4 protein abundance correlated with features of metastasis. A METTL3 small molecule inhibitor markedly diminished both EML4 m6A and protein abundance, and efficiently suppressed lung metastases in vivo. Our findings unveil a dynamic and functional epitranscriptomic landscape in lung adenocarcinoma, pinpointing the hyper-methylation of EML4 as a key driver of tumor metastasis.

2024-05-31 | GSE263726 | GEO

The N6-methyladenosine Epitranscriptomic Landscape of Lung Adenocarcinoma [RIP-seq]

2024-05-31 | GSE263725 | GEO

Epitranscriptomic map of N6-methyladenosine circular RNAs in the spinal cord of morphine-tolerant rats

Project description:Epitranscriptomic map of N6-methyladenosine circular RNAs in the spinal cord of morphine-tolerant rats

| PRJNA821901 | ENA

N6-methyladenosine Modification of lncRNA Pvt1 Governs Epidermal Stemness

Project description:Dynamic chemical modifications of RNA represent novel and fundamental mechanisms that regulate stemness and tissue homeostasis. Rejuvenation and wound repair of mammalian skin are sustained by epidermal progenitor cells, which are localized within the basal layer of the skin epidermis. N6-methyladenosine (m6A) is one of the most abundant modifications found in eukaryotic mRNA and lncRNA (long non-coding RNA). In this report, we survey changes of m6A RNA methylomes upon epidermal differentiation, and identify Pvt1, a lncRNA whose m6A modification is critically involved in sustaining stemness of epidermal progenitor cells. With genome-editing and a mouse genetics approach, we show that ablation of m6A methyltransferase or Pvt1 impairs the self-renewal and wound healing capability of skin. Mechanistically, methylation of Pvt1 transcripts enhances its interaction with MYC and stabilizes the MYC protein in epidermal progenitor cells. Our study presents a global view of epitranscriptomic dynamics that occur during epidermal differentiation and identifies the m6A modification of Pvt1 as a key signaling event involved in skin tissue homeostasis and wound repair.

2021-02-01 | GSE165912 | GEO

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