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Potent ATM kinase inhibitor (IC50 = 6.3 nM). Exhibits little to no nonspecific target effects against a panel of 229 protein kinases; displays similar target selectivity to KU 55933 (Cat. No. 3544). Inhibits migration and invasion of human glioma cells in vitro.
Sold with the permission of AstraZeneca.
External Portal Information
Chemicalprobes.org is a portal that offers independent guidance on the selection and/or application of small molecules for research. The use of KU 60019 is reviewed on the chemical probes website.
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The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Golding et al (2009) Improved ATM kinase inhibitor KU-60019 radiosensitizes glioma cells, compromises Ins, AKT and ERK prosurvival signaling, and inhibits migration and invasion. Mol.Cancer Ther. 8 2894 PMID: 19808981
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Keywords: KU 60019, KU 60019 supplier, Astrazeneca, KU60019, atm, kinases, ataxia, telangiectasia, mutated, potent, inhibitors, inhibits, ATM, &, ATR, Kinase, Checkpoint, Control, Kinases, 4176, Tocris Bioscience
14 Citations for KU 60019
Citations are publications that use Tocris products. Selected citations for KU 60019 include:
Mehta et al (2015) Human papillomaviruses activate and recruit SMC1 cohesin proteins for the differentiation-dependent life cycle through association with CTCF insulators. PLoS Pathog 11 e1004763 PMID: 25875106
Montané and Menand (2013) ATP-competitive mTOR kinase inhibitors delay plant growth by triggering early differentiation of meristematic cells but no developmental patterning change. J Biol Chem 64 4361 PMID: 23963679
Gautam (2013) The kinase activity of ataxia-telangiectasia mutated interferes with adenovirus E4 mutant DNA replication. J Virol 87 8687 PMID: 23740981
Koo et al (2015) RNA polymerase III regulates cytosolic RNA:DNA hybrids and intracellular microRNA expression. Nucleic Acids Res 290 7463 PMID: 25623070
Parplys et al (2015) NUCKS1 is a novel RAD51AP1 paralog important for homologous recombination and genome stability. Cell Cycle 43 9817 PMID: 26323318
Davari et al (2014) Checkpoint kinase 2 is required for efficient immunoglobulin diversification. Cell Cycle 13 3659 PMID: 25483076
Barton et al (2014) Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1. J Cell Biol 206 877 PMID: 25267294
Yang et al (2018) Cell type-dependent bimodal p53 activation engenders a dynamic mechanism of chemoresistance. Sci Adv 4 eaat5077 PMID: 30585287
Rass et al (2013) Ataxia telangiectasia mutated (ATM) is dispensable for endonuclease I-SceI-induced homologous recombination in mouse embryonic stem cells. J Biol Chem 288 7086 PMID: 23355489
Ryl et al (2017) Cell-Cycle Position of Single MYC-Driven Cancer Cells Dictates Their Susceptibility to a Chemotherapeutic Drug. Cell Syst 5 237 PMID: 28843484
Jaiswal et al (2017) ATM/Wip1 activities at chromatin control Plk1 re-activation to determine G2 checkpoint duration. EMBO J 36 2161 PMID: 28607002
Deng et al (2016) Replication of an Autonomous Human Parvovirus in Non-dividing Human Airway Epithelium Is Facilitated through the DNA Damage and Repair Pathways. PLoS Pathog 12 e1005399 PMID: 26765330
Müllers et al (2014) Nuclear translocation of Cyclin B1 marks the restriction point for terminal cell cycle exit in G2 phase. Cell Cycle 13 2733 PMID: 25486360
Wu et al (2014) Selenoprotein H suppresses cellular senescence through genome maintenance and redox regulation. J Biol Chem 289 34378 PMID: 25336634
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Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.