Zobrazeno 1 - 10
of 13
pro vyhledávání: '"Jiri Bartek"'
Autor:
Christian T. Carson, Darwin V. Lee, Jiri Lukas, Matthew D. Weitzman, Nicole I. Orazio, Seema S. Lakdawala, Caroline E. Lilley, Jiri Bartek, Junghae Suh, Felipe D. Araujo, Simon Bekker-Jensen
Publikováno v:
The EMBO Journal. 28:652-662
The protein kinases ataxia-telangiectasia mutated (ATM) and ATM-Rad3 related (ATR) are activated in response to DNA damage, genotoxic stress and virus infections. Here we show that during infection with wild-type adenovirus, ATR and its cofactors RPA
Autor:
Claudia Lukas, Stephen P. Jackson, Jiri Lukas, Jiri Bartek, Jacob Falck, Ali Jazayeri, Graeme C. M. Smith
Publikováno v:
Nature Cell Biology. 8:37-45
It is generally thought that the DNA-damage checkpoint kinases, ataxia-telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR), work independently of one another. Here, we show that ATM and the nuclease activity of meiotic recombination 11 (Mre1
Autor:
Maxwell Sehested, Jiri Bartek, Niels E. Skakkebæk, Jiri Lukas, Michael B. Kastan, Christopher J. Bakkenist, Jirina Bartkova, Ewa Rajpert-De Meyts
Publikováno v:
Cell Cycle. 4:838-845
The ATM kinase is a tumor suppressor and key regulator of biological responses to DNA damage. Cultured cells respond to genotoxic insults that induce DNA double-strand breaks by prompt activation of ATM through its autophosphorylation on serine 1981.
Publikováno v:
Molecular and Cellular Biology. 24:6350-6361
DNA damage induces cell cycle arrest and DNA repair or apoptosis in proliferating cells. Terminally differentiated cells are permanently withdrawn from the cell cycle and partly resistant to apoptosis. To investigate the effects of genotoxic agents i
Autor:
Kum Kum Khanna, Bin-Bing S. Zhou, Randi G. Syljuåsen, Magtouf Gatei, Kienan I. Savage, Jiri Bartek, Katie Sloper, Claus Storgaard Sørensen, Karen Hobson, Jacob Falck, Jiri Lukas
Publikováno v:
Journal of Biological Chemistry. 278:14806-14811
In mammals, the ATM (ataxia-telangiectasia-mutated) and ATR (ATM and Rad3-related) protein kinases function as critical regulators of the cellular DNA damage response. The checkpoint functions of ATR and ATM are mediated, in part, by a pair of checkp
Autor:
Jacob Falck, Jiri Bartek, Randi G. Syljuåsen, Bin-Bing S. Zhou, Jiri Lukas, Kum Kum Khanna, Lars Rönnstrand, Tine Schroeder, Claus Storgaard Sørensen
Publikováno v:
University of Copenhagen
Chk1 kinase coordinates cell cycle progression and preserves genome integrity. Here, we show that chemical or genetic ablation of human Chk1 triggered supraphysiological accumulation of the S phase-promoting Cdc25A phosphatase, prevented ionizing rad
Publikováno v:
Nature. 410:842-847
When exposed to ionizing radiation (IR), eukaryotic cells activate checkpoint pathways to delay the progression of the cell cycle. Defects in the IR-induced S-phase checkpoint cause 'radioresistant DNA synthesis', a phenomenon that has been identifie
Autor:
Jiri Lukas, Michael A. Strauss, Klaus Hansen, Jirina Bartkova, Selina Khan, Lars Rönnstrand, Minna Thullberg, Jiri Bartek
Publikováno v:
Lund University
University of Copenhagen
University of Copenhagen
p16(INK4a), p15(INK4b), p18(INK4c) and p19(INK4d) comprise a family of cyclin-dependent kinase inhibitors and tumor suppressors. We report that the INK4 proteins share the ability to arrest cells in G1, and interact with CDK4 or CDK6 with similar avi
Autor:
Claudia Lukas, Jiri Bartek, Simon Bekker-Jensen, David C. Schultz, Yosef Shiloh, Yaron Galanty, Yael Ziv, Jiri Lukas, Yoichi Taya, Dana Bielopolski
Publikováno v:
Nature cell biology. 8(8)
The cellular DNA-damage response is a signaling network that is vigorously activated by cytotoxic DNA lesions, such as double-strand breaks (DSBs)1. The DSB response is mobilized by the nuclear protein kinase ATM, which modulates this process by phos
Autor:
Christopher J. Bakkenist, Zuzana Horejsi, Jiri Bartek, Jiri Lukas, Jacob Falck, Michael B. Kastan
Publikováno v:
Oncogene. 23(17)
The ATM kinase is a tumour suppressor and a key activator of genome integrity checkpoints in mammalian cells exposed to ionizing radiation (IR) and other insults that elicit DNA double-strand breaks (DSBs). In response to IR, autophosphorylation on s