Hilde Loge Nilsen

Image of Hilde Loge Nilsen
Norwegian version of this page
Phone +47 67963922
Mobile phone +47 93246618
Username
Visiting address Norway Sykehusveien 25 Akershus University Hospital Epigen B2 1478 Lørenskog
Postal address Akershus universitetssykehus 1478 LØRENSKOG

Academic Interests

Mechanisms of DNA and RNA quality control in human disease.

Positions held

  • 2013 - present:  Professor Department of Clinical Molecular Biology
  • 2009 - 2013:  Assistant Director, Biotechnology Centre of Oslo.
  • 2006 - present:  Problem-based learning supervisor, Medical Faculty, University of Oslo.
  • 2004 - 2013:  Group leader, “DNA Repair”, Biotechnology Centre of Oslo.

Education

  • 2000 - 2004:  Post doctoral fellow, Cancer Research UK.
  • 2000:  Dr. ing. from the Norwegian University of Science and Technology (NTNU), Trondheim, Norway

Research Interests

We are interested in the quality control mechanisms that maintain function of DNA and RNA throughout the lifetime of cells and organisms.

DNA repair enzymes remove damaged or inappropriate bases from DNA. Historically, studies of DNA repair has been motivated by the need for these mechanisms in order to prevent mutations - changes in the genetic code. Studies of DNA repair is therefore important in order to understand how cancer develops and how cancer can be treated. In recent years it has become clear that DNA repair enzymes have many important functions in cells other than to prevent mutations, most importantly in neurobiology to prevent neurodegenerative diseases. We have also recently demonstrated that some DNA repair proteins also contribute to RNA quality control. 

Aims:

  • To study whether DNA damage and mutations may act as a driver of tumorigenesis
  • To study how DNA repair mechanisms protect us from premature aging and age-related neurodegenerative diseases
  • To study how DNA repair proteins contribute to RNA quality Control

Research achievements

  • We have revealed mutation signatures associated with failure to repair uracil via the Base Excision repair pathway (Alsøe et al., 2017)
  • We have uncovered a mechanism by which failure to repair nuclear DNA can lead to progressive mitochondrial dysfunction and neurodegeneration (Fang et al., 2014; Fang et al 2016)
  • We have demonstrated that the DNA repair enzyme SMUG1 removes damaged bases from RNA and contribute to RNA quality control (Jobert et al., 2013)
  • We have identified a novel mechanism for induction of autophagy by the chemotherapeutic agent 5-fluorouracil (Erdelyi et al., 2011; SenGupta 2013)
  • We have described transcriptomic and proteomic changes that compensate for the lack of DNA repair in C. elegans and contribute to maintain normal lifespan (Fensgård et al, 2010; Skjeldam et al., 2010; Arczewska et al., 2012; Lans et al 2013; Kassahun et al., 2017)
  • We demonstrated that DNA repair enzymes act to initiate cellular signaling cascades leading to activation of apoptosis (Dengg et al., 2006)
Tags: DNA repair, DNA damage, Neurodegeneration, Ageing, Cancer
Published Sep. 4, 2013 12:57 PM - Last modified Jan. 2, 2018 2:59 PM