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Hendrik Marks

Researcher at Radboud University Nijmegen

Publications -  64
Citations -  5474

Hendrik Marks is an academic researcher from Radboud University Nijmegen. The author has contributed to research in topics: Embryonic stem cell & Chromatin. The author has an hindex of 30, co-authored 60 publications receiving 4740 citations. Previous affiliations of Hendrik Marks include University Medical Center Groningen & Wageningen University and Research Centre.

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The Transcriptional and Epigenomic Foundations of Ground State Pluripotency

TL;DR: It is suggested that transcriptional potentiation and a permissive chromatin context characterize the ground state and that exit from it may not require a metastable intermediate or multilineage priming.
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Quantitative Interaction Proteomics and Genome-wide Profiling of Epigenetic Histone Marks and Their Readers

TL;DR: The authors' data reveal a highly adapted interplay between chromatin marks and their associated protein complexes, and reading specific trimethyl-lysine sites by specialized complexes appears to be a widespread mechanism to mediate gene expression.
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Sequential ChIP-bisulfite sequencing enables direct genome-scale investigation of chromatin and DNA methylation cross-talk

TL;DR: ChIP-bisulfite-sequencing was used in this article to quantitatively assess DNA methylation patterns associated with chromatin modifications or chromatin-associated factors directly, and the results showed that H3K27me3 and DNA are compatible throughout most of the genome, except for CpG islands, where these two marks are mutually exclusive.
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Mll2 is required for h3k4 trimethylation on bivalent promoters in embryonic stem cells, whereas mll1 is redundant

TL;DR: It is shown that Mll2, one of the six Set1/Trithorax-type H3K4 methyltransferases in mammals, is required for trimethylation of bivalent promoters in mouse embryonic stem cells and proposed that MLL2 is the pioneer trimethyltransferase for promoter definition in the naïve epigenome and that Polycomb group action on bivalent promoter blocks the premature establishment of active, Set1C-bound, promoters.