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Karl Agger

Researcher at University of Copenhagen

Publications -  21
Citations -  5161

Karl Agger is an academic researcher from University of Copenhagen. The author has contributed to research in topics: Histone methyltransferase & Histone Demethylases. The author has an hindex of 16, co-authored 21 publications receiving 4754 citations. Previous affiliations of Karl Agger include Novo Nordisk Foundation & European Institute of Oncology.

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UTX and JMJD3 are histone H3K27 demethylases involved in HOX gene regulation and development.

TL;DR: It is shown that the human JmjC-domain-containing proteins UTX and JMJD3 demethylate tri-methylated Lys 27 on histone H3, and the results suggest that H3K27me3 dem methylation regulated by UTX/JMJD3 proteins is essential for proper development.
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The putative oncogene GASC1 demethylates tri- and dimethylated lysine 9 on histone H3

TL;DR: In addition to identifying GASC1 as a histone trimethyl demethylase, this work suggests a model for how this enzyme might be involved in cancer development, and proposes it as a target for anti-cancer therapy.
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Erasing the methyl mark: histone demethylases at the center of cellular differentiation and disease

TL;DR: The emerging biochemical and biological functions of the histone demethylases are reviewed and their potential involvement in human diseases, including cancer, is discussed.
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RBP2 belongs to a family of demethylases, specific for tri-and dimethylated lysine 4 on histone 3

TL;DR: It is demonstrated that the JARID1 proteins RBP2, PLU1, and SMCX are histone demethylases specific for di- and trimethylated histone 3 lysine 4 (H3K4) and that mutation or RNAi depletion of the C. elegans JARid1 homolog rbr-2 leads to increased levels of H3K 4me3 during larval development and defects in vulva formation.
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The H3K27me3 demethylase JMJD3 contributes to the activation of the INK4A–ARF locus in response to oncogene- and stress-induced senescence

TL;DR: It is shown that expression of the histone H3 Lys 27 (H3K27) demethylase JMJD3 is induced upon activation of the RAS-RAF signaling pathway and contributes to the transcriptional activation of p16INK4A in human diploid fibroblasts.