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1,184 results for “m6A”
Analysis of variant-dependent m6A modifications within the Human genome
<p>Interactive and machine-readable results produced by the <a href="https://github.com/cumbof/m6Ad-SNVs" target="_blank" rel="noopener">m6Ad-SNVs</a> tool to asses if m6A-distal SNVs affect DRACH site accessibility, specifically by evaluating the alteration of base-pairing of nucleotides within segments of the DRACH motif.</p> <p>These results contain the predicted m6Ad-SNV candidates with the length of the reference and m6Ad-SNV-containing alternate sequences limited to 250 base pairs. This constraint has been applied to maintain the reliability of the results predicted by RNAFold (<a href="https://www.tbi.univie.ac.at/RNA/">ViennaRNA</a> package). The sequence composition contains up to 100 base pairs from 3'UTRs, with the remaining base pairs limited to the last two exons.</p>
Summary statistics data for "Genetic Analyses Support the Contribution of mRNA N6-methyladenosine (m6A) Modification to Human Diseases Heritability"
<p>We included the summary statistics data associated with our manuscript "<strong>Genetic Analyses Support the Contribution of mRNA <em>N</em><sup>6</sup>-methyladenosine (m<sup>6</sup>A) Modification to Human Diseases Heritability". </strong></p> <p>We also included the newly imputed genotype data for the 60 YRI individuals involved in our study, the joint m<sup>6</sup>A peaks tested (locations of the molecular phetnotype in BED12 format) and normalized log odds ratio (enrichment) of these joint peaks (molecular phenotype data). </p>
m6A-TWAS weights for "Genetic Analyses Support the Contribution of mRNA N6-methyladenosine (m6A) Modification to Human Diseases Heritability"
<p>We included the m6A-TWAS weights (trained using FUSION) for our manuscript "Genetic Analyses Support the Contribution of mRNA <em>N</em>6-methyladenosine (m6A) Modification to Human Diseases Heritability". </p> <p>This dataset is a supplement to the m6A QTL summary statistics data and imputed genotype data at https:// doi.org/10.5281/zenodo.3870952.</p>
Genome and gene annotation for yeast strain SK1 used in "Deciphering the "m6A Code" via Antibody-Independent Quantitative Profiling"
<p>Genome and gene annotation used in "Deciphering the “m6A Code” via Antibody-Independent Quantitative Profiling" provided by Schraga Schwartz from his time at the Broad Institute.</p>
Fibertools: fast and accurate m6A calling using single-molecule long-read sequencing (ML data)
<p>Fibertools is a convolutional neural network that permits the fast and accurate identification of endogenous and exogenous N6-methyladenine (m6A)-marked bases using single-molecule long-read sequencing.<strong> </strong>This dataset (ML data) provides training and validation data for training fibertools supervised and semi-supervised CNN models for three long-read chemistries.</p>
PCB126 exposure revealed alterations in m6A RNA modifications in transcripts associated with AHR activation
<p>Chemical modifications of proteins, DNA and RNA moieties play critical roles in regulating gene expression. Emerging evidence suggests the RNA modifications (epitranscriptomics) have substantive roles in basic biological processes. One of the most common modifications in mRNA and noncoding RNAs is <i>N</i><sup>6</sup>-methyladenosine (m6A). In a subset of mRNAs, m<sup>6</sup>A sites are preferentially enriched near stop codons, in 3′ UTRs, and within exons, suggesting an important role in the regulation of mRNA processing and function including alternative splicing and gene expression. Very little is known about the effect of environmental chemical exposure on m6A modifications. As many of the commonly occurring environmental contaminants alter gene expression profiles and have detrimental effects on physiological processes, it is important to understand the effects of exposure on this important layer of gene regulation. Hence, the objective of this study was to characterize the acute effects of developmental exposure to PCB126, an environmentally relevant dioxin-like PCB, on m6A methylation patterns. We exposed zebrafish embryos to PCB126 for 6 hours starting from 72 hours post-fertilization and profiled m6A RNA using methylated RNA immunoprecipitation followed by sequencing (MeRIP-seq). Our analysis revealed 117 and 217 m6A peaks in the DMSO and PCB126 samples (FDR 5%), respectively. The majority of the peaks were preferentially located around the 3'UTR and stop codons. Statistical analysis revealed 15 m6A marked transcripts to be differentially methylated by PCB126 exposure. These include transcripts that are known to be activated by AHR agonists (e.g., <i>ahrra</i>, <i>tiparp</i>, <i>nfe2l2b) as well as others that are important for normal development (vgf, cebpd, sned1). These results suggest that</i> environmental chemicals such as dioxin-like PCBs could affect developmental gene expression patterns by altering m6A levels. Further studies are necessary to understand the functional consequences of exposure-associated alterations in m6A levels.</p>
m6A-dependent 7-dehydrocholesterol reductase facilitates bladder cancer metastasis via cAMP/PKA/FAK axis
<p><span>Cholesterol homeostasis dysregulation </span><span>appears</span><span> in multiple tumors. However, the specific processes that cause abnormal cholesterol metabolism to affect the invasion and metastasis of bladder cancer (BC) are still unclear. In our investigation, we found a notable rise in the expression of 7-dehydrocholesterol reductase (DHCR7), a key enzyme involved in the synthesis of cholesterol, within BC tissues in comparison to normal tissues and correlated to the invasion and metastasis of BC. This elevated expression of DHCR7 in BC was attributed to the decreased degradation of mRNA mediated by YTHDF2. We discovered that DHCR7 </span><span>plays</span><span> a role in promoting bladder cancer invasion and metastasis </span><span>by</span><span> activating the cAMP-PKA-FAK pathway. Specifically, DHCR7 was found to increase the levels of cAMP by enhancing cholesterol content in lipid rafts, thereby facilitating the transduction of signaling pathways mediated by cAMP receptors. Additionally, DHCR7 was found to enhance the cAMP signaling pathway by reducing the concentration of 7-DHC and promoting the transcription of GIPR. Overall, our findings demonstrated that DHCR7 plays a crucial role in BC invasion and metastasis by modulating cholesterol synthesis and cAMP signaling pathways. Furthermore, AY9944, which acts as an inhibitor of DHCR7, shows promise as a viable therapeutic strategy for the suppression of invasion and metastasis in BC.</span></p>
RNA-seq Data for Bacteroides fragilis Toxin Suppresses METTL3-Mediated m6A Modification in Macrophage to Promote Inflammatory Bowel Disease
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SUPREM: an engineered non-site-specific m6A RNA methyltransferase with highly improved efficiency
<p>The deposited files are the ancestral sequence reconstruction dataset of M.EcoGII.</p>
m6A modifications regulate intestinal immunity and rotavirus infection
<p>N6-methyladenosine (m6A) is an abundant mRNA modification and affects many biological processes. However, how m6A levels are regulated during physiological or pathological processes such as virus infections, and the <em>in vivo</em> function of m6A in the intestinal immune defense against virus infections are largely unknown. Here, we uncover a novel antiviral function of m6A modification during rotavirus (RV) infection in small bowel intestinal epithelial cells (IECs). We found that rotavirus infection induced global m6A modifications on mRNA transcripts by down-regulating the m6a eraser ALKBH5. Mice lacking the m6A writer enzymes METTL3 in IECs (<em>Mettl3</em><sup>ΔIEC</sup>) were resistant to RV infection and showed increased expression of interferons (IFNs) and IFN-stimulated genes (ISGs). Using RNA-sequencing and m6A RNA immuno-precipitation (RIP)-sequencing, we identified IRF7, a master regulator of IFN responses, as one of the primary m6A targets during virus infection. In the absence of METTL3, IECs showed increased <em>Irf7</em> mRNA stability and enhanced type I and III IFN expression. Deficiency in IRF7 attenuated the elevated expression of IFNs and ISGs and restored susceptibility to RV infection in <em>Mettl3</em><sup>ΔIEC</sup> mice. Moreover, the global m6A modification on mRNA transcripts declined with age in mice, with a significant drop from 2 weeks to 3 weeks post birth, which likely has broad implications for the development of intestinal immune system against enteric viruses early in life. Collectively, we demonstrated a novel host m6A-IRF7-IFN antiviral signaling cascade that restricts rotavirus infection <em>in vivo</em>.</p>
PCB126 exposure revealed alterations in m6A RNA modifications in transcripts associated with AHR activation
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m6A modifications regulate intestinal immunity and rotavirus infection
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RNA m6A methylation in unilateral ureteral ligations model
<p>Chronic kidney disease (CKD) is a high incidence disease. Renal fibrosis is the ultimate pathological pathway for chronic kidney diseases leading to end-stage renal failure. There is currently no effective treatment to prevent the renal fibrosis. Renal EMT is a key mechanism of renal fibrosis. Recent evidence suggests m<sup>6</sup>A modification in RNA can regulate EMT in tumor cells. However, a role of m<sup>6</sup>A RNA modification in renal fibrosis has not been reported. Therefore, we investigate whether m<sup>6</sup>A RNA methylation plays an important role in the epithelial-to-mesenchymal transition (EMT) process of renal fibrosis. Unilateral ureteral ligations were performed in C57BL/6 mice to establish a mouse model of renal fibrosis and TGF-b intervention was used in HK2 cells to establish a cellular model of renal fibrosis. The effects of m<sup>6</sup>A and the role of <i>Mettl14 </i>on kidney disease and HK2 cells were studied. </p>
scRNA-seq data for "Bacteroides fragilis toxin suppresses METTL3-Mediated m6A modification in macrophage to promote inflammatory bowel disease"
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m6A modification inhibits miRNA intracellular function favouring their extracellular export and the cell-to-cell communication
<p>Epitranscriptomics represents a new layer of gene expression regulation. Specifically, N6-methyladenosine (m6A) regulates RNA maturation, stability, degradation, and translation. Regarding miRNAs, while it has been reported that m6A impact their biogenesis, no evidence is yet provided on their function. Here we show that m6A modification on specific miRNAs weakens their coupling to AGO2, impairs their function on target mRNAs, determines their delivery into extracellular vesicles (EVs) and provides functional information to receiving cells. Mechanistically, the intracellular functional impairment is caused by m6A-mediated inhibition of AGO2/miRNA interaction, the EV-loading is favoured by m6A-mediated recognition by the RBP hnRNPA2B1, the EV-miRNAs function in the receiving cell requires their FTO-mediated demethylation. Consequently, cells express specific miRNAs that do not impact endogenous transcripts but provide regulatory information for cell-to-cell communication. This highlights that a further level of complexity should be considered when relating cellular dynamics to specific miRNAs.</p>
Interactive Structural Analysis of KH3-4 Didomains of IGF2BPs with Preferred RNA Motif Having m6A through Dynamics Simulation Studies
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RNA m6A methylation in unilateral ureteral ligations model
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Dynamics of m6A RNA methylome during leukemogenesis reveals a role of PRMT6-MFSD2A signaling axis in maintaining AML stem cells.[RIP-seq]
GEO Series GSE218610. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
m6A-seq analysis of Wild Type and Mettl3-/- BMDMs (bone-marrow-derived macrophages) Transcriptomes
GEO Series GSE146140. Mus musculus. 8 samples. Type: Methylation profiling by high throughput sequencing.
Single-nucleus multiomic mapping of m6A methylome and transcriptome in native populations of cells with sn-m6A-CT
GEO Series GSE217256. Homo sapiens; Mus musculus. 36 samples. Type: Other; Expression profiling by high throughput sequencing.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
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DANDI Archive for NWB datasets
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
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