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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

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.

Research Group

Name Titel
Jiri Bartek Professor
Jirina Bartkova Senior researcher
Andrea Björkman Postdoc
Jaime Andrés Espinoza Ruiz Postdoc
Johana Fernandez Martinez Laboratory technician
Dimitris Kanellis Postdoc
Bennie Lemmens Postdoc
Mikael Lindström Senior researcher
Per Moberg Research coordinator
Ann-Sofie Nilsson Biomedical scientist
Kenneth Schou Visiting researcher
Asimina Zisi PhD student


Selected Publications

Alcohol-abuse drug disulfiram targets cancer via p97 segregase adaptor NPL4.
Skrott Z, Mistrik M, Andersen KK, Friis S, Majera D, Gursky J, et al
Nature 2017 12;552(7684):194-199

Chronic p53-independent p21 expression causes genomic instability by deregulating replication licensing.
Galanos P, Vougas K, Walter D, Polyzos A, Maya-Mendoza A, Haagensen EJ, et al
Nat. Cell Biol. 2016 07;18(7):777-89

Tumors overexpressing RNF168 show altered DNA repair and responses to genotoxic treatments, genomic instability and resistance to proteotoxic stress.
Chroma K, Mistrik M, Moudry P, Gursky J, Liptay M, Strauss R, et al
Oncogene 2017 04;36(17):2405-2422

TOPBP1 regulates RAD51 phosphorylation and chromatin loading and determines PARP inhibitor sensitivity.
Moudry P, Watanabe K, Wolanin KM, Bartkova J, Wassing IE, Watanabe S, et al
J. Cell Biol. 2016 Feb;212(3):281-8

A Synergistic Interaction between Chk1- and MK2 Inhibitors in KRAS-Mutant Cancer.
Dietlein F, Kalb B, Jokic M, Noll EM, Strong A, Tharun L, et al
Cell 2015 Jul;162(1):146-59

REV7 counteracts DNA double-strand break resection and affects PARP inhibition.
Xu G, Chapman JR, Brandsma I, Yuan J, Mistrik M, Bouwman P, et al
Nature 2015 May;521(7553):541-544

ATR mediates a checkpoint at the nuclear envelope in response to mechanical stress.
Kumar A, Mazzanti M, Mistrik M, Kosar M, Beznoussenko GV, Mironov AA, et al
Cell 2014 Jul;158(3):633-46

ATR prohibits replication catastrophe by preventing global exhaustion of RPA.
Toledo LI, Altmeyer M, Rask MB, Lukas C, Larsen DH, Povlsen LK, et al
Cell 2013 Nov;155(5):1088-103

JMJD1C demethylates MDC1 to regulate the RNF8 and BRCA1-mediated chromatin response to DNA breaks.
Watanabe S, Watanabe K, Akimov V, Bartkova J, Blagoev B, Lukas J, et al
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.
Yamada M, Watanabe K, Mistrik M, Vesela E, Protivankova I, Mailand N, et al
Genes Dev. 2013 Nov;27(22):2459-72

The DNA-damage response in human biology and disease.
Jackson SP, Bartek J
Nature 2009 Oct;461(7267):1071-8

Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints.
Bartkova J, Rezaei N, Liontos M, Karakaidos P, Kletsas D, Issaeva N, et al
Nature 2006 Nov;444(7119):633-7

External funding

Vetenskapsrådet

Cancerfonden

Radiumhemmets forskningsfonder