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  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1186/s13059-020-02249-z.

Title:
N6-methyladenosine dynamics in neurodevelopment and aging, and its potential role in Alzheimer’s disease | Genome Biology
Description:
Background N6-methyladenosine (m6A) modification is known to impact many aspects of RNA metabolism, including mRNA stability and translation, and is highly prevalent in the brain. Results We show that m6A modification displays temporal and spatial dynamics during neurodevelopment and aging. Genes that are temporally differentially methylated are more prone to have mRNA expression changes and affect many pathways associated with nervous system development. Furthermore, m6A shows a distinct tissue-specific methylation profile, which is most pronounced in the hypothalamus. Tissue-specific methylation is associated with an increase in mRNA expression and is associated with tissue-specific developmental processes. During the aging process, we observe significantly more m6A sites as age increases, in both mouse and human. We show a high level of overlap between mouse and human; however, humans at both young and old ages consistently show more m6A sites compared to mice. Differential m6A sites are found to be enriched in alternative untranslated regions of genes that affect aging-related pathways. These m6A sites are associated with a strong negative effect on mRNA expression. We also show that many Alzheimer-related transcripts exhibit decreased m6A methylation in a mouse model of Alzheimer’s disease, which is correlated with reduced protein levels. Conclusions Our results suggest that m6A exerts a critical function in both early and late brain development in a spatio-temporal fashion. Furthermore, m6A controls protein levels of key genes involved in Alzheimer’s disease-associated pathways, suggesting that m6A plays an important role in aging and neurodegenerative disease.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Education
  • Science
  • Technology & Computing

Content Management System {šŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {šŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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How Does Link.springer.com Make Money? {šŸ’ø}

The income method remains a mystery to us.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com might be cashing in, but we can't detect the method they're using.

Keywords {šŸ”}

pubmed, methylation, article, google, scholar, cas, mrna, genes, rna, levels, brain, compared, weeks, mice, fig, central, expression, transcripts, disease, protein, mouse, aging, alzheimers, methylated, gene, development, utr, differentially, role, file, xfad, wang, neurodevelopment, sites, additional, human, differential, data, zhang, show, regulation, week, analysis, alternative, involved, function, liu, showing, nmethyladenosine, mettl,

Topics {āœ’ļø}

ubiquitin-positive tau-negative inclusions ß-actin house-keeping gene eye-specific gmr-gal4 driver /articles/dataset/m6a_a_lc-ms-ms/13356179 n6-methyladenosine-dependent regulation anti-n6-methyladenosine antibody rna n6-methyladenosine methyltransferase lc-ms/ms m6a quantification lc-ms/ms m6a data 5-hmc-mediated epigenetic dynamics intraneuronal beta-amyloid aggregates exploring deep-sequencing data article download pdf steady-state mrna levels n6-methyladenosine dynamics lc-ms/ms quantification including dna methylation pre-built reference file central south university 28-cm-height plastic tubes tissue-specific developmental processes lc-ms/ms confirmed lc/ms-ms poly facilitates hippocampus-dependent learning neuron-cellular interactions early similar tissue-specific methylation gov/geo/query/acc rna-seq data served replicate rna-seq data happ/ps1 ad models hippocampus-specific methylation correlates performed deep rna-seq surviving high-quality reads spatial-specific m6a methylation regulates mammalian spermatogenesis refined rip-seq protocol /ashafik1/shafik_et_al_codes/tree/main [75] rna-seq data processing affect aging-related pathways human hnrnp a2/b1 analyze merip-seq data m6a_a_lc-ms-ms hypothalamus-specific methylation occurs lc-ms/ms protein-protein interactions age-related neurodegenerative disease + enriched mrna-seq libraries tissue-specific methylation privacy choices/manage cookies methyladenosine-modified rna

Questions {ā“}

Schema {šŸ—ŗļø}

WebPage:
      mainEntity:
         headline:N6-methyladenosine dynamics in neurodevelopment and aging, and its potential role in Alzheimer’s disease
         description:N6-methyladenosine (m6A) modification is known to impact many aspects of RNA metabolism, including mRNA stability and translation, and is highly prevalent in the brain. We show that m6A modification displays temporal and spatial dynamics during neurodevelopment and aging. Genes that are temporally differentially methylated are more prone to have mRNA expression changes and affect many pathways associated with nervous system development. Furthermore, m6A shows a distinct tissue-specific methylation profile, which is most pronounced in the hypothalamus. Tissue-specific methylation is associated with an increase in mRNA expression and is associated with tissue-specific developmental processes. During the aging process, we observe significantly more m6A sites as age increases, in both mouse and human. We show a high level of overlap between mouse and human; however, humans at both young and old ages consistently show more m6A sites compared to mice. Differential m6A sites are found to be enriched in alternative untranslated regions of genes that affect aging-related pathways. These m6A sites are associated with a strong negative effect on mRNA expression. We also show that many Alzheimer-related transcripts exhibit decreased m6A methylation in a mouse model of Alzheimer’s disease, which is correlated with reduced protein levels. Our results suggest that m6A exerts a critical function in both early and late brain development in a spatio-temporal fashion. Furthermore, m6A controls protein levels of key genes involved in Alzheimer’s disease-associated pathways, suggesting that m6A plays an important role in aging and neurodegenerative disease.
         datePublished:2021-01-05T00:00:00Z
         dateModified:2021-01-05T00:00:00Z
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            Epitranscriptomics
            m6A
            Neurodevelopment
            Aging
            Alzheimer’s
            Regulation of mRNA levels
            Regulation of protein levels
            Alternative 3′UTR
            Animal Genetics and Genomics
            Human Genetics
            Plant Genetics and Genomics
            Microbial Genetics and Genomics
            Bioinformatics
            Evolutionary Biology
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ScholarlyArticle:
      headline:N6-methyladenosine dynamics in neurodevelopment and aging, and its potential role in Alzheimer’s disease
      description:N6-methyladenosine (m6A) modification is known to impact many aspects of RNA metabolism, including mRNA stability and translation, and is highly prevalent in the brain. We show that m6A modification displays temporal and spatial dynamics during neurodevelopment and aging. Genes that are temporally differentially methylated are more prone to have mRNA expression changes and affect many pathways associated with nervous system development. Furthermore, m6A shows a distinct tissue-specific methylation profile, which is most pronounced in the hypothalamus. Tissue-specific methylation is associated with an increase in mRNA expression and is associated with tissue-specific developmental processes. During the aging process, we observe significantly more m6A sites as age increases, in both mouse and human. We show a high level of overlap between mouse and human; however, humans at both young and old ages consistently show more m6A sites compared to mice. Differential m6A sites are found to be enriched in alternative untranslated regions of genes that affect aging-related pathways. These m6A sites are associated with a strong negative effect on mRNA expression. We also show that many Alzheimer-related transcripts exhibit decreased m6A methylation in a mouse model of Alzheimer’s disease, which is correlated with reduced protein levels. Our results suggest that m6A exerts a critical function in both early and late brain development in a spatio-temporal fashion. Furthermore, m6A controls protein levels of key genes involved in Alzheimer’s disease-associated pathways, suggesting that m6A plays an important role in aging and neurodegenerative disease.
      datePublished:2021-01-05T00:00:00Z
      dateModified:2021-01-05T00:00:00Z
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      license:http://creativecommons.org/publicdomain/zero/1.0/
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      keywords:
         Epitranscriptomics
         m6A
         Neurodevelopment
         Aging
         Alzheimer’s
         Regulation of mRNA levels
         Regulation of protein levels
         Alternative 3′UTR
         Animal Genetics and Genomics
         Human Genetics
         Plant Genetics and Genomics
         Microbial Genetics and Genomics
         Bioinformatics
         Evolutionary Biology
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      name:Qing Dai
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      name:Kinga Pajdzik
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            name:University of Chicago
            address:
               name:Department of Chemistry, University of Chicago, Chicago, USA
               type:PostalAddress
            type:Organization
      name:Yangping Li
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               name:Department of Human Genetics, School of Medicine, Emory University, Atlanta, USA
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      name:Yunhee Kang
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               type:PostalAddress
            type:Organization
      name:Bing Yao
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               type:PostalAddress
            type:Organization
      name:Hao Wu
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            address:
               name:Department of Biostatistics and Bioinformatics, School of Public Health, Emory University, Atlanta, USA
               type:PostalAddress
            type:Organization
      name:Chuan He
      affiliation:
            name:University of Chicago
            address:
               name:Department of Chemistry, University of Chicago, Chicago, USA
               type:PostalAddress
            type:Organization
      name:Emily G. Allen
      affiliation:
            name:Emory University
            address:
               name:Department of Human Genetics, School of Medicine, Emory University, Atlanta, USA
               type:PostalAddress
            type:Organization
      name:Ranhui Duan
      affiliation:
            name:Central South University
            address:
               name:Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, China
               type:PostalAddress
            type:Organization
      name:Peng Jin
      url:http://orcid.org/0000-0001-6137-6659
      affiliation:
            name:Emory University
            address:
               name:Department of Human Genetics, School of Medicine, Emory University, Atlanta, USA
               type:PostalAddress
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      email:[email protected]
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      name:Department of Human Genetics, School of Medicine, Emory University, Atlanta, USA
      name:Department of Human Genetics, School of Medicine, Emory University, Atlanta, USA
      name:Department of Biostatistics and Bioinformatics, School of Public Health, Emory University, Atlanta, USA
      name:Department of Chemistry, University of Chicago, Chicago, USA
      name:Department of Chemistry, University of Chicago, Chicago, USA
      name:Department of Human Genetics, School of Medicine, Emory University, Atlanta, USA
      name:Department of Human Genetics, School of Medicine, Emory University, Atlanta, USA
      name:Department of Human Genetics, School of Medicine, Emory University, Atlanta, USA
      name:Department of Biostatistics and Bioinformatics, School of Public Health, Emory University, Atlanta, USA
      name:Department of Chemistry, University of Chicago, Chicago, USA
      name:Department of Human Genetics, School of Medicine, Emory University, Atlanta, USA
      name:Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, China
      name:Department of Human Genetics, School of Medicine, Emory University, Atlanta, USA

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