B
Benjamin Leblanc
Researcher at University of Copenhagen
Publications - 12
Citations - 5336
Benjamin Leblanc is an academic researcher from University of Copenhagen. The author has contributed to research in topics: Chromatin & Chromosome conformation capture. The author has an hindex of 10, co-authored 12 publications receiving 4746 citations. Previous affiliations of Benjamin Leblanc include Centre national de la recherche scientifique.
Papers
More filters
Journal ArticleDOI
Three-Dimensional Folding and Functional Organization Principles of the Drosophila Genome
Tom Sexton,Eitan Yaffe,Ephraim Kenigsberg,Frédéric Bantignies,Benjamin Leblanc,Michael Hoichman,Hugues Parrinello,Amos Tanay,Giacomo Cavalli +8 more
TL;DR: A high-resolution chromosomal contact map derived from a modified genome-wide chromosome conformation capture approach applied to Drosophila embryonic nuclei is presented, laying the foundation for detailed studies of chromosome structure and function in a genetically tractable system.
Journal ArticleDOI
Genome Regulation by Polycomb and Trithorax Proteins
Bernd Schuettengruber,Daniel Chourrout,Michel Vervoort,Michel Vervoort,Benjamin Leblanc,Giacomo Cavalli +5 more
TL;DR: Polycomb group (PcG) and trithorax group (trxG) proteins are critical regulators of numerous developmental genes and recent work suggests that PcG-mediated gene silencing involves noncoding RNAs and the RNAi machinery.
Journal ArticleDOI
Polycomb-dependent regulatory contacts between distant Hox loci in Drosophila
Frédéric Bantignies,Virginie Roure,Itys Comet,Benjamin Leblanc,Bernd Schuettengruber,Jerome Bonnet,Vanessa Tixier,André Mas,Giacomo Cavalli +8 more
TL;DR: It is shown that genes of the two Hox complexes can interact within nuclear PcG bodies in tissues where they are corepressed, resulting in the exacerbation of homeotic phenotypes in sensitized genetic backgrounds.
Journal ArticleDOI
EZH2 is a potential therapeutic target for H3K27M-mutant pediatric gliomas
Faizaan Mohammad,Simon Weissmann,Benjamin Leblanc,Deo Prakash Pandey,Jonas W. Højfeldt,Itys Comet,Chunqin Zheng,Jens Vilstrup Johansen,Nicolas Rapin,Bo T. Porse,Andrey Tvardovskiy,Andrey Tvardovskiy,Ole N. Jensen,Ole N. Jensen,Nagore G. Olaciregui,Cinzia Lavarino,Mariona Suñol,Carmen de Torres,Jaume Mora,Angel M. Carcaboso,Kristian Helin +20 more
TL;DR: Results show that residual PRC2 activity is required for the proliferation of H3K27M-expressing DIPGs, and that inhibition of EZH2 is a potential therapeutic strategy for the treatment of these tumors.
Journal ArticleDOI
Gene Silencing Triggers Polycomb Repressive Complex 2 Recruitment to CpG Islands Genome Wide
TL;DR: The results show that it is the transcriptional state that governs PRC2 binding, and it is proposed that it binds by default to nontranscribed CGI genes to maintain their silenced state and to protect cell identity.