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Florian Lienert

Researcher at Friedrich Miescher Institute for Biomedical Research

Publications -  8
Citations -  2206

Florian Lienert is an academic researcher from Friedrich Miescher Institute for Biomedical Research. The author has contributed to research in topics: DNA methylation & Epigenomics. The author has an hindex of 6, co-authored 6 publications receiving 2004 citations. Previous affiliations of Florian Lienert include University of Basel.

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DNA-binding factors shape the mouse methylome at distal regulatory regions

TL;DR: It is shown that DNA-binding factors locally influence DNA methylation, enabling the identification of active regulatory regions and shows that neuronal and stem-cell methylomes are dependent on each other, as cell-type-specific LMRs are occupied by cell- type-specific transcription factors.
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Identification of genetic elements that autonomously determine DNA methylation states

TL;DR: It is demonstrated that proximal sequence elements are both necessary and sufficient for regulating DNA methylation and reveal basic constraints of this regulation.
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Methylation-Dependent and -Independent Genomic Targeting Principles of the MBD Protein Family

TL;DR: Functional binding maps for the methyl-CpG-binding domain (MBD) family of proteins reveal methylation-dependent and -independent binding modes and revise current models of DNA methylation readout through MBD proteins.
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Genomic prevalence of heterochromatic H3K9me2 and transcription do not discriminate pluripotent from terminally differentiated cells.

TL;DR: The dynamics of the transcriptome and an abundant heterochromatic histone modification, dimethylation of histone H3 at lysine 9 (H3K9me2), during neuronal differentiation of embryonic stem cells are reported, which suggests that cellular differentiation entails local rather than global changes in epigenetic repression and transcriptional activity.
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Accessibility of the Drosophila genome discriminates PcG repression, H4K16 acetylation and replication timing

TL;DR: DNA accessibility is increased at active promoters and chromosomal regions that are hyperacetylated at H4K16, particularly at the male X chromosome, suggesting that transcriptional dosage compensation is facilitated by permissive chromatin structure.