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Ulrike Boenisch
Researcher at Max Planck Society
Publications - 7
Citations - 489
Ulrike Boenisch is an academic researcher from Max Planck Society. The author has contributed to research in topics: Epigenome & PRC2. The author has an hindex of 3, co-authored 7 publications receiving 393 citations.
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Journal ArticleDOI
Paternal Diet Defines Offspring Chromatin State and Intergenerational Obesity
Anita Öst,Anita Öst,Adelheid Lempradl,Eduard Casas,Melanie Weigert,Theodor Tiko,Merdin Deniz,Lorena Pantano,Ulrike Boenisch,Pavel M. Itskov,Marlon Stoeckius,Marius Ruf,Nikolaus Rajewsky,Gunter Reuter,Nicola Iovino,Carlos Ribeiro,Mattias Alenius,Steffen Heyne,Tanya Vavouri,J. Andrew Pospisilik +19 more
TL;DR: A Drosophila model of paternal-diet-induced intergenerational metabolic reprogramming (IGMR) is presented and evidence that a similar system may regulate obesity susceptibility and phenotype variation in mice and humans is found.
Journal ArticleDOI
The Polycomb-Dependent Epigenome Controls β Cell Dysfunction, Dedifferentiation, and Diabetes.
Tess Tsai Hsiu Lu,Steffen Heyne,Erez Dror,Eduard Casas,Laura Leonhardt,Laura Leonhardt,Thorina Boenke,Chih-Hsiang Yang,Sagar,Laura Arrigoni,Kevin Dalgaard,Raffaele Teperino,Lennart Enders,Madhan Selvaraj,Marius Ruf,Sunil Jayaramaiah Raja,Huafeng Xie,Ulrike Boenisch,Stuart H. Orkin,Francis C. Lynn,Brad G. Hoffman,Dominic Grün,Tanya Vavouri,Adelheid Lempradl,J. Andrew Pospisilik +24 more
TL;DR: Deep epigenome mapping with single-cell transcriptomics finds two chromatin-state signatures that track β cell dysfunction in mice and humans: ectopic activation of bivalent Polycomb-silenced domains and loss of expression at an epigenomically unique class of lineage-defining genes.
Journal ArticleDOI
DOT1L Activity Promotes Proliferation and Protects Cortical Neural Stem Cells from Activation of ATF4-DDIT3-Mediated ER Stress In Vitro
Deborah Roidl,Nicole Hellbach,Patrick Piero Bovio,Alejandro Villarreal,Stefanie Heidrich,Sigrun Nestel,Björn Grüning,Ulrike Boenisch,Tanja Vogel +8 more
TL;DR: Investigation of the function of DOT1L in neural stem cells of the cerebral cortex found that loss of H3K79me2 at the Atf4‐ and Ddit3‐promoters appears to mark a point‐of‐no‐return that activates the death program in NSCs.
Journal ArticleDOI
RELACS: a novel in-nuclei barcoding strategy for high-throughput ChIP-seq
Posted ContentDOI
Ultra-parallel ChIP-seq by barcoding of intact nuclei
Laura Arrigoni,Al-Hasani H,Fidel Ramírez,Ilaria Panzeri,Devon Ryan,Diana Santacruz,Nadia Kress,Andrew Pospisilik,Ulrike Boenisch,Thomas Manke +9 more
TL;DR: A novel method for ultra-parallelized high-throughput ChIP-seq that employs barcoding of chromatin within intact nuclei extracted from different sources, for maximal comparability and significant workload reduction.