Valentyn Oksenych

Bilde av Valentyn Oksenych
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Besøksadresse Sognsvannsveien 20 Rikshospitalet 0372 Oslo
Postadresse OUS HF Rikshospitalet Postboks 4950 Nydalen 0424 Oslo

Academic interests

DNA in our cells is constantly damaged by various internal and external factors. To maintain genomic stability, the cells developed multiple DNA repair pathways. Mutations in DNA repair genes lead to disorders in human. Non-Homologous End-Joining (NHEJ) fixes the DNA double-strand breaks (DSB) throughout the cell cycle. NHEJ is required for the development of immune and nervous systems and to suppress medulloblastoma.

NHEJ consists of Ku70, Ku80, XLF, XRCC4, DNA Ligase 4, DNA-PKcs, Artemis, XLS/PAXX, APLF, Mri/Cyren. There is a complex genetic interaction between the NHEJ factors (e.g., Oksenych et al., PNAS, 2013; Xing et al., DNA repair, 2017; Castaneda-Zegarra et al., DNA repair, 2019; Xing and Oksenych, FEBS open bio, 2019; Castaneda-Zegarra et al., Aging, 2020;  Castaneda-Zegarra et al., Scandinavian Journal of Immunology, 2020). 

In response to DNA damage, there is a complex process that includes the activation of multiple enzymes and modifications of proteins, such as histones surrounding the DSBs. This process is called the DNA damage response (DDR) pathway. It is facilitated by protein kinases ATM and DNA-PKcs, scaffold proteins MDC1 and 53BP1, ubiquitin-ligases RNF8 and RNF168, and many other proteins. During the DDR, histones are phosphorylated, ubiquitylated, methylated, acetylated, SUMOylated, NEDDylated, etc (Zha et al., Nature, 2011; Oksencyh et al., PNAS, 2012; Kumar et al., DNA repair, 2014; Beck et al., Biomolecules, 2020). I am attempting to understand the complexity of DDR, as well as its role in the development of immune system and in cancer suppression.

Both NHEJ and DDR pathways are involved in immune system development, including the V(D)J recombination in developing B and T lymphocytes, and the Class Switch Recombination (CSR) in mature B cells.

Translocations associated with V(D)J recombination and class switch recombination (CSR) can be detected using High Throughput Genome-Wide Translocation sequencing (HTGTS). I collaborate with researchers at Karolinska Institutet and Harvard Medical School to develop HTGTS-based assays using primary human B cells.

Several drug candidates were identified to be used in cancer and immune disease treatments. I collaborate with researchers at UiO and local Hospitals to validate and select the best options for further translation to the clinic. 


2020-Now       Researcher. University of Oslo, Norway

2020:              Researcher. University of Tromsø, Norway

2018-2020      Research visit. Karolinska Institutet, Sweden

2015-2020      Researcher, principal investigator. NTNU - Trondheim, Norway

2014-2015      Postdoc. University of Copenhagen, Denmark

2010-2014      Postdoc. Harvard Medical School, USA

2005-2009      PhD candidate. IGBMC, University of Strasbourg, France

Past projects and awards

2020-2021      Karolinska Institutet (KI Stiftelser och Fonder)

2020-2021      Health Authority of Central Norway

2019-2022      PhD position (SO), award in innovation, NTNU, Norway

2018-2019      NTNU PES and POS grants, Norway

2018-2019      Research Council of Norway, FRIPRO

2017-2021      Outstanding Academic Fellow Award, NTNU, Norway

2017-2020      Norwegian Cancer Society, Open call

2016-2019      Research Council of Norway, FRIMEDBIO

2016-2018      Research Council of Norway, FRIPRO

2016-2018      Health Authority of Central Norway

2015-2017      Lundbeck Fellowship, University of Copenhagen, Denmark

2009               Anti-Cancer Research Association (ARC), France

2008               Anti-Cancer Research Association (ARC), France

2005               Mobility grant, IBB - Academy of Science, Warsaw, Poland

Emneord: B cells, DNA repair, mouse models, Genetics, Immunology
Publisert 27. nov. 2020 14:17 - Sist endret 2. des. 2020 19:04