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Nicolas Rapin

Researcher at University of Copenhagen

Publications -  50
Citations -  5496

Nicolas Rapin is an academic researcher from University of Copenhagen. The author has contributed to research in topics: CEBPA & Transcription factor. The author has an hindex of 25, co-authored 49 publications receiving 4191 citations. Previous affiliations of Nicolas Rapin include Technical University of Denmark & Finsen Laboratory.

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An atlas of active enhancers across human cell types and tissues

TL;DR: It is shown that enhancers share properties with CpG-poor messenger RNA promoters but produce bidirectional, exosome-sensitive, relatively short unspliced RNAs, the generation of which is strongly related to enhancer activity.
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Computational Immunology Meets Bioinformatics: The Use of Prediction Tools for Molecular Binding in the Simulation of the Immune System

TL;DR: An agent-based simulator of the immune response is extended such that it represents pathogens, as well as lymphocytes receptors, by means of their amino acid sequences and makes use of bioinformatics methods for T and B cell epitope prediction, which shows that the simulator produces dynamics that are stable and consistent with basic immunological knowledge.
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BloodSpot: a database of gene expression profiles and transcriptional programs for healthy and malignant haematopoiesis.

TL;DR: The database now includes 23 high-quality curated data sets relevant to normal and malignant blood formation and, in addition, it has assembled and built a unique integrated data set, BloodPool, which contains more than 2000 samples assembled from six independent studies on acute myeloid leukemia.
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Loss of TET2 in hematopoietic cells leads to DNA hypermethylation of active enhancers and induction of leukemogenesis

TL;DR: It is proposed that TET2 prevents leukemic transformation by protecting enhancers from aberrant DNA methylation and that it is the combined silencing of several tumor suppressor genes in Tet2 mutated hematopoietic cells that contributes to increased stem cell proliferation and leukemogenesis.