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  Genome-wide Kinase-Chromatin Interactions Reveal the Regulatory Network of ERK Signaling in Human Embryonic Stem Cells

Göke, J., Chan, Y. S., Yan, J. L., Vingron, M., & Ng, H. H. (2013). Genome-wide Kinase-Chromatin Interactions Reveal the Regulatory Network of ERK Signaling in Human Embryonic Stem Cells. Molecular Cell, 50(6), 844-855. doi:DOI 10.1016/j.molcel.2013.04.030.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0019-0B22-F Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0019-0B26-7
Genre: Journal Article

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 Creators:
Göke, J.1, Author              
Chan, Y. S., Author
Yan, J. L., Author
Vingron, M.2, Author              
Ng, H. H., Author
Affiliations:
1Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, Ihnestr. 73, 14195 Berlin, Germany, ou_1433547              
2Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society, Ihnestr, 73, 14195 Berlin, Germany, ou_1479639              

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Free keywords: transcriptional regulation cycle progression gene-expression self-renewal phosphorylation pluripotency growth circuitry cascades pathways
 Abstract: The extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase signal-transduction cascade is one of the key pathways regulating proliferation and differentiation in development and disease. ERK signaling is required for human embryonic stem cells' (hESCs') self-renewing property. Here, we studied the convergence of the ERK signaling cascade at the DNA by mapping genome-wide kinase-chromatin interactions for ERK2 in hESCs. We observed that ERK2 binding occurs near noncoding genes and histone, cell-cycle, metabolism, and pluripotency-associated genes. We find that the transcription factor ELK1 is essential in hESCs and that ERK2 co-occupies promoters bound by ELK1. Strikingly, promoters bound by ELK1 without ERK2 are occupied by Polycomb group proteins that repress genes involved in lineage commitment. In summary, we propose a model wherein extracellular-signaling-stimulated proliferation and intrinsic repression of differentiation are integrated to maintain the identity of hESCs.

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Language(s): eng - English
 Dates: 2013-05-302013-06-27
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: DOI 10.1016/j.molcel.2013.04.030
ISSN: 1097-2765
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Title: Molecular Cell
Source Genre: Journal
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Publ. Info: Cambridge, Mass. : Cell Press
Pages: - Volume / Issue: 50 (6) Sequence Number: - Start / End Page: 844 - 855 Identifier: ISSN: 1097-2765
CoNE: https://pure.mpg.de/cone/journals/resource/954925610929