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. Of particular interest is discovery of targets and markers for personalized cancer treatment and finding novel components or mechanisms of genome integrity maintenance. The lab uses a variety of approaches including state of the art cell and molecular biology techniques, genetic and chemical biology screens, immunohistochemistry as well as advanced methods in imaging.
|Jirina Bartkova||Senior researcher|
|Johana Fernandez Martinez||Laboratory technician|
|Mikael Lindström||Senior researcher|
|Kaveh Moazemi||PhD student|
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):541-4
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