Emmanouela Repapi joined the Computational Biology Research Group in January 2014. Since then she has worked on a variety of projects ranging from studying splicing alterations in myelodysplastic syndromes to being involved in the analysis of datasets with the aim of understanding the mechanisms underlying the endothelial to hematopoietic transition. In her time in the Weatherall Institute of Molecular Medicine (WIMM) she has been focusing on the analysis of all types of RNA Sequencing data, including single-cell analysis. She has also been teaching the RNA-Seq course in the WIMM, along with Nicki Gray. Dr Repapi completed her DPhil at the Ludwig Institute for Cancer Research at the University of Oxford working on the identification and analysis of single nucleotide polymorphisms (SNPs) that affect cancer in humans. She was involved in numerous projects, working with clinical and genetic data of different types of cancer including chronic lymphocytic leukemia, melanoma and pancreatic cancer. Her first degree was in Applied Mathematics at the National Technical University of Athens before completing an MSc in Applied Statistics at the University of Oxford. Prior to her PhD, she worked as a training fellow in Genetic Epidemiology at the University of Leicester conducting a meta-analysis of Genome Wide Association Studies (GWAS) for pulmonary function.
Impact of spliceosome mutations on RNA splicing in myelodysplasia: dysregulated genes/pathways and clinical associations.
Pellagatti A. et al, (2018), Blood, 132, 1225 - 1240
Canonical Notch signaling is dispensable for adult steady-state and stress myelo-erythropoiesis.
Duarte S. et al, (2018), Blood, 131, 1712 - 1719
Single-cell analysis reveals the continuum of human lympho-myeloid progenitor cells.
Karamitros D. et al, (2018), Nat immunol, 19, 85 - 97
CD1a presentation of endogenous antigens by group 2 innate lymphoid cells.
Hardman CS. et al, (2017), Sci immunol, 2
Hepcidin is regulated by promoter-associated histone acetylation and HDAC3.
Pasricha S-R. et al, (2017), Nat commun, 8