Jiri Bartek Group
Cells employ an extensive network of DNA damage response (DDR) processes to maintain genome integrity and to promote survival after exposure to genotoxic stresses. Distinct DNA repair pathways respond to different types of damage, while cell cycle checkpoints provide the time that is needed to repair DNA lesions. Research in the Bartek lab focuses on various mechanistic aspects of the DDR and DNA repair pathways.
Research in the Bartek lab focuses on various mechanistic aspects of the DDR and DNA repair pathways. Of particular interest is discovery of targets and markers for personalized cancer treatment and finding novel components or mechanisms of genome integrity maintenance. Another of our long-term goals is to further unravel the principles of ribosome biogenesis surveillance and to understand the dynamics and the finer details of the p53 pathway in sensing ribosome dysfunction, and how ribosomal stress crosstalk with the DNA damage response.
|Jirina Bartkova||Senior researcher|
|Jaime Andrés Espinoza Ruiz||Postdoc|
|Johana Fernandez Martinez||Laboratory technician|
|Mikael Lindström||Senior researcher|
|Kaveh Moazemi||PhD student|
|Per Moberg||Research coordinator|
|Ann-Sofie Nilsson||Biomedical scientist|
|Kenneth Schou||Visiting researcher|
|Asimina Zisi||R&D trainee|
“Alcohol-abuse drug disulfiram targets cancer via p97 segregase adaptor NPL4”
Zdenek Skrott, Martin Mistrik, Klaus Kaae Andersen, Søren Friis, Dusana Majera, Jan Gursky, Tomas Ozdian, Jirina Bartkova, Zsofia Turi, Pavel Moudry, Marianne Kraus, Martina Michalova, Jana Vaclavkova, Petr Dzubak, Ivo Vrobel, Pavla Pouckova, Jindrich Sedlacek, Andrea Miklovicova, Anne Kutt, Jing Li, Jana Mattova, Christoph Driessen, Q. Ping Dou, Jørgen Olsen, Marian Hajduch, Boris Cvek, Raymond J. Deshaies & Jiri Bartek
Nature, online 6 December 2017, doi: 10.1038/nature25016
Chronic p53-independent p21 expression causes genomic instability by deregulating replication licensing.
Nat. Cell Biol. 2016 Jul;18(7):777-89
TOPBP1 regulates RAD51 phosphorylation and chromatin loading and determines PARP inhibitor sensitivity.
J. Cell Biol. 2016 Feb;212(3):281-8
A Synergistic Interaction between Chk1- and MK2 Inhibitors in KRAS-Mutant Cancer.
Cell 2015 Jul;162(1):146-59
REV7 counteracts DNA double-strand break resection and affects PARP inhibition.
Nature 2015 May;521(7553):541-544
ATR mediates a checkpoint at the nuclear envelope in response to mechanical stress.
Cell 2014 Jul;158(3):633-46
ATR prohibits replication catastrophe by preventing global exhaustion of RPA.
Cell 2013 Nov;155(5):1088-103
JMJD1C demethylates MDC1 to regulate the RNF8 and BRCA1-mediated chromatin response to DNA breaks.
Nat. Struct. Mol. Biol. 2013 Dec;20(12):1425-33
ATR-Chk1-APC/CCdh1-dependent stabilization of Cdc7-ASK (Dbf4) kinase is required for DNA lesion bypass under replication stress.
Genes Dev. 2013 Nov;27(22):2459-72
The DNA-damage response in human biology and disease.
Nature 2009 Oct;461(7267):1071-8
Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints.
Nature 2006 Nov;444(7119):633-7