Oscar Fernandez-Capetillo Group

Professor

Oscar Fernandez-Capetillo

Organizational unit: Oscar Fernandez-Capetillo's Group
E-mail: oscar.fernandez-capetillo@ki.se

Oscar Fernandez-Capetillo's profile page.

Research Interests

DNA damage is a known cause of cancer and ageing. In this context, drugs that either generate DNA damage or inhibit DNA repair have shown good efficacy in the treatment of tumors, and are the current standard of care in several cases. Still, our knowledge of the specific synthetic lethal interactions that can enhance the efficacy of these treatments is somewhat rudimentary and there is room for improvement. I have previously been involved in the development of DNA repair inhibitors and help them arise clinical phases. At KI, I want to further pursue these translational activities by integrating our research with the national platforms available in the area of drug development. While our research will still have an angle towards DNA damage and repair, we will also explore other health-relevant areas such as the development of immune-modulators or new strategies to treat amyotrophic lateral sclerosis.

Group Members

Bomi JungPostdoc
Daniela HühnPostdoc
Jordi Carreras PuigvertProject manager
Kirsten TschapaldaAssociated
Louise LidemalmLaboratory technician
Maria HäggbladResearch engineer
Oscar Fernandez-CapetilloProfessor
Per MobergResearch coordinator

Key Publications

A Genome-wide CRISPR Screen Identifies CDC25A as a Determinant of Sensitivity to ATR Inhibitors.
Ruiz S, Mayor-Ruiz C, Lafarga V, Murga M, Vega-Sendino M, Ortega S, et al
Mol. Cell 2016 Apr;62(2):307-13

USP7 is a SUMO deubiquitinase essential for DNA replication.
Lecona E, Rodriguez-Acebes S, Specks J, Lopez-Contreras A, Ruppen I, Murga M, et al
Nat. Struct. Mol. Biol. 2016 Apr;23(4):270-7

NSMCE2 suppresses cancer and aging in mice independently of its SUMO ligase activity.
Jacome A, Gutierrez-Martinez P, Schiavoni F, Tenaglia E, Martinez P, Rodríguez-Acebes S, et al
EMBO J. 2015 Nov;34(21):2604-19

Limiting replication stress during somatic cell reprogramming reduces genomic instability in induced pluripotent stem cells.
Ruiz S, Lopez-Contreras A, Gabut M, Marion R, Gutierrez-Martinez P, Bua S, et al
Nat Commun 2015 ;6():8036

Increased Rrm2 gene dosage reduces fragile site breakage and prolongs survival of ATR mutant mice.
Lopez-Contreras A, Specks J, Barlow J, Ambrogio C, Desler C, Vikingsson S, et al
Genes Dev. 2015 Apr;29(7):690-5

The maternal side of Fanconi Anemia.
Ruiz S, Fernandez-Capetillo O
Mol. Cell 2014 Sep;55(6):803-4