M
Michael Rebhan
Researcher at Novartis
Publications - 24
Citations - 4754
Michael Rebhan is an academic researcher from Novartis. The author has contributed to research in topics: Cellular differentiation & DNA methylation. The author has an hindex of 12, co-authored 22 publications receiving 4184 citations. Previous affiliations of Michael Rebhan include Friedrich Miescher Institute for Biomedical Research & Weizmann Institute of Science.
Papers
More filters
Journal ArticleDOI
Distribution, silencing potential and evolutionary impact of promoter DNA methylation in the human genome.
Michael Weber,Ines Hellmann,Michael B. Stadler,Liliana Ramos,Svante Pääbo,Michael Rebhan,Dirk Schübeler +6 more
TL;DR: Results show that promoter sequence and gene function are major predictors of promoter methylation states and that inactive unmethylated CpG island promoters show elevated levels of dimethylation of Lys4 of histone H3, suggesting that this chromatin mark may protect DNA from methylation.
Journal ArticleDOI
Lineage-specific polycomb targets and de novo DNA methylation define restriction and potential of neuronal progenitors
Fabio Mohn,Michael Weber,Michael Rebhan,Tim Roloff,Jens Richter,Michael B. Stadler,Miriam Bibel,Dirk Schübeler +7 more
TL;DR: A model how de novo DNA methylation and dynamic switches in Polycomb targets restrict pluripotency and define the developmental potential of progenitor cells is suggested.
Journal ArticleDOI
GeneCards: integrating information about genes, proteins and diseases
Journal ArticleDOI
GeneCards: a novel functional genomics compendium with automated data mining and query reformulation support.
TL;DR: A model for a new type of topic-specific overview resource that provides efficient access to distributed information is developed, which is a freely accessible Web resource that offers one hypertext 'card' for each of the more than 7000 human genes that have an approved gene symbol published by the HUGO/GDB nomenclature committee.
Journal ArticleDOI
Calcium-activated chloride channel ANO1 promotes breast cancer progression by activating EGFR and CAMK signaling
Adrian Britschgi,Anke Bill,Heike Brinkhaus,Christopher Rothwell,Ieuan Clay,Stephan Duss,Michael Rebhan,Pichai Raman,Chantale T. Guy,Kristie Wetzel,Elizabeth George,M. Oana Popa,Sarah Lilley,Hedaythul Choudhury,Martin Gosling,Louis Wang,Stephanie Fitzgerald,Jason Borawski,Jonathan Baffoe,Mark Labow,L. Alex Gaither,Mohamed Bentires-Alj +21 more
TL;DR: The results highlight the involvement of the ANO1 chloride channel in tumor progression and provide insights into oncogenic signaling in human cancers with 11q13 amplification, thereby establishing ANO 1 as a promising target for therapy in these highly prevalent tumor types.