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We began analyzing https://www.nature.com/articles/ng.1036, but it redirected us to https://www.nature.com/articles/ng.1036. The analysis below is for the second page.

Title[redir]:
A chromatin-modifying function of JNK during stem cell differentiation | Nature Genetics
Description:
Dirk Schübeler, Michael Stadler and colleagues show that the c-Jun NH2-terminal kinase (JNK) binds directly to active promoters during the differentiation of stem cells to neurons and targets histone H3 serine 10 for phosphorylation. Signaling mediates cellular responses to extracellular stimuli. The c-Jun NH2-terminal kinase (JNK) pathway exemplifies one subgroup of the mitogen-activated protein (MAP) kinases, which, besides having established functions in stress response, also contribute to development by an unknown mechanism1,2,3,4. We show by genome-wide location analysis that JNK binds to a large set of active promoters during the differentiation of stem cells into neurons. JNK-bound promoters are enriched with binding motifs for the transcription factor NF-Y but not for AP-1. NF-Y occupies these predicted sites, and overexpression of dominant-negative NF-YA reduces the JNK presence on chromatin. We find that histone H3 Ser10 (H3S10) is a substrate for JNK, and JNK-bound promoters are enriched for H3S10 phosphorylation. Inhibition of JNK signaling in post-mitotic neurons reduces phosphorylation at H3S10 and the expression of target genes. These results establish MAP kinase binding and function on chromatin at a novel class of target genes during stem cell differentiation.

Matching Content Categories {📚}

  • Education
  • Science
  • Telecommunications

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

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Traffic Estimate {📈}

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


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Keywords {🔍}

article, google, scholar, cas, cell, nature, jnk, histone, phosphorylation, biol, access, stem, cells, kinase, protein, data, kinases, development, content, nat, mol, research, map, open, embryonic, cookies, differentiation, signaling, transcription, nfy, regulation, science, manuscript, privacy, function, analysis, stadler, schübeler, pathway, neurons, chromatin, expression, genes, gene, signal, genet, sci, basel, european, information,

Topics {✒️}

nature portfolio permissions reprints privacy policy open access database nf-κb–dependent gene expression open software development c-jun nh2-terminal kinase author information authors c-jun n-terminal kinases advertising cytokine-induced gene expression european research council social media novartis research foundation jun n-terminal kinase dominant-negative nf-ya reduces nature 461 nature 438 nature 423 nature tools lineage-specific polycomb targets italy biomedical research mitogen-activated protein kinases stress-activated kinase 1/2 msk-dependent h3k27me3s28 phosphorylation cell type-dependent control transcription factor-binding profiles map kinase–mediated phosphorylation research springerlink instant access myc-dependent transcriptional activation genome-wide location analysis mitogen-activated protein permissions hp1-chromatin binding p38 mapk pathways annexin a1 expression stem cell differentiation quantitative genomics facility friedrich miescher institute iκb kinase-α drosophila thorax development early embryonic neurogenesis privacy scaffold protein revealed dominant-negative analogs transcription factor nf short dna sequences

Questions {❓}

  • AP-1—the Jun proteins: oncogenes or tumor suppressors in disguise?
  • Histone H3 phosphorylation: universal code or lineage specific dialects?
  • Phosphorylation of serine 10 in histone H3, what for?

Schema {🗺️}

WebPage:
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         headline:A chromatin-modifying function of JNK during stem cell differentiation
         description:Dirk Schübeler, Michael Stadler and colleagues show that the c-Jun NH2-terminal kinase (JNK) binds directly to active promoters during the differentiation of stem cells to neurons and targets histone H3 serine 10 for phosphorylation. Signaling mediates cellular responses to extracellular stimuli. The c-Jun NH2-terminal kinase (JNK) pathway exemplifies one subgroup of the mitogen-activated protein (MAP) kinases, which, besides having established functions in stress response, also contribute to development by an unknown mechanism1,2,3,4. We show by genome-wide location analysis that JNK binds to a large set of active promoters during the differentiation of stem cells into neurons. JNK-bound promoters are enriched with binding motifs for the transcription factor NF-Y but not for AP-1. NF-Y occupies these predicted sites, and overexpression of dominant-negative NF-YA reduces the JNK presence on chromatin. We find that histone H3 Ser10 (H3S10) is a substrate for JNK, and JNK-bound promoters are enriched for H3S10 phosphorylation. Inhibition of JNK signaling in post-mitotic neurons reduces phosphorylation at H3S10 and the expression of target genes. These results establish MAP kinase binding and function on chromatin at a novel class of target genes during stem cell differentiation.
         datePublished:2011-12-18T00:00:00Z
         dateModified:2011-12-18T00:00:00Z
         pageStart:94
         pageEnd:100
         sameAs:https://doi.org/10.1038/ng.1036
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            Cell signalling
            Chromatin
            Gene regulation
            Stem-cell differentiation
            Biomedicine
            general
            Human Genetics
            Cancer Research
            Agriculture
            Gene Function
            Animal Genetics and Genomics
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      headline:A chromatin-modifying function of JNK during stem cell differentiation
      description:Dirk Schübeler, Michael Stadler and colleagues show that the c-Jun NH2-terminal kinase (JNK) binds directly to active promoters during the differentiation of stem cells to neurons and targets histone H3 serine 10 for phosphorylation. Signaling mediates cellular responses to extracellular stimuli. The c-Jun NH2-terminal kinase (JNK) pathway exemplifies one subgroup of the mitogen-activated protein (MAP) kinases, which, besides having established functions in stress response, also contribute to development by an unknown mechanism1,2,3,4. We show by genome-wide location analysis that JNK binds to a large set of active promoters during the differentiation of stem cells into neurons. JNK-bound promoters are enriched with binding motifs for the transcription factor NF-Y but not for AP-1. NF-Y occupies these predicted sites, and overexpression of dominant-negative NF-YA reduces the JNK presence on chromatin. We find that histone H3 Ser10 (H3S10) is a substrate for JNK, and JNK-bound promoters are enriched for H3S10 phosphorylation. Inhibition of JNK signaling in post-mitotic neurons reduces phosphorylation at H3S10 and the expression of target genes. These results establish MAP kinase binding and function on chromatin at a novel class of target genes during stem cell differentiation.
      datePublished:2011-12-18T00:00:00Z
      dateModified:2011-12-18T00:00:00Z
      pageStart:94
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         Cell signalling
         Chromatin
         Gene regulation
         Stem-cell differentiation
         Biomedicine
         general
         Human Genetics
         Cancer Research
         Agriculture
         Gene Function
         Animal Genetics and Genomics
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                     name:Faculty of Science, University of Basel, Basel, Switzerland
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            name:Dirk Schübeler
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                     name:Faculty of Science, University of Basel, Basel, Switzerland
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         name:Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland
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      name:Dirk Schübeler
      affiliation:
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            address:
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               name:Department of Biosystems Science and Engineering, Eidgenössische Technische Hochschule (ETH) Zürich, Basel, Switzerland
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      name:Department of Biosystems Science and Engineering, Eidgenössische Technische Hochschule (ETH) Zürich, Basel, Switzerland
      name:Faculty of Science, University of Basel, Basel, Switzerland
      name:Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland
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Social Networks {👍}(2)

External Links {🔗}(243)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.js
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {📦}

  • Crossref

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