TOPping up ATR activity

Research output: Contribution to journal › Comment/debate › Research › peer-review

Standard

TOPping up ATR activity. / Bartek, Jiri; Mailand, Niels.

In: Cell, Vol. 124, No. 5, 10.03.2006, p. 888-90.

Research output: Contribution to journal › Comment/debate › Research › peer-review

Harvard

Bartek, J & Mailand, N 2006, 'TOPping up ATR activity', Cell, vol. 124, no. 5, pp. 888-90. https://doi.org/10.1016/j.cell.2006.02.029

APA

Bartek, J., & Mailand, N. (2006). TOPping up ATR activity. Cell, 124(5), 888-90. https://doi.org/10.1016/j.cell.2006.02.029

Vancouver

Bartek J, Mailand N. TOPping up ATR activity. Cell. 2006 Mar 10;124(5):888-90. https://doi.org/10.1016/j.cell.2006.02.029

Author

Bartek, Jiri ; Mailand, Niels. / TOPping up ATR activity. In: Cell. 2006 ; Vol. 124, No. 5. pp. 888-90.

Bibtex

@article{8746ca0952bf4fb0888d8f1a5a97d7f6,
title = "TOPping up ATR activity",
abstract = "The nuclear protein kinase ATR is a key regulator of genome integrity that functions at checkpoints for damaged or incompletely replicated DNA. In this issue of Cell, Kumagai et al. (2006) shed light on the molecular mechanism that controls ATR. They report that a physical interaction between ATR and a distinct domain of TopBP1 greatly enhances ATR kinase activity.",
keywords = "Animals, Ataxia Telangiectasia Mutated Proteins, Carrier Proteins, Cell Cycle Proteins, DNA Repair, DNA-Binding Proteins, Enzyme Activation, Gene Expression Regulation, Humans, Models, Genetic, Nuclear Proteins, Protein-Serine-Threonine Kinases, Xenopus Proteins",
author = "Jiri Bartek and Niels Mailand",
year = "2006",
month = mar,
day = "10",
doi = "10.1016/j.cell.2006.02.029",
language = "English",
volume = "124",
pages = "888--90",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "5",

}

RIS

TY - JOUR

T1 - TOPping up ATR activity

AU - Bartek, Jiri

AU - Mailand, Niels

PY - 2006/3/10

Y1 - 2006/3/10

N2 - The nuclear protein kinase ATR is a key regulator of genome integrity that functions at checkpoints for damaged or incompletely replicated DNA. In this issue of Cell, Kumagai et al. (2006) shed light on the molecular mechanism that controls ATR. They report that a physical interaction between ATR and a distinct domain of TopBP1 greatly enhances ATR kinase activity.

AB - The nuclear protein kinase ATR is a key regulator of genome integrity that functions at checkpoints for damaged or incompletely replicated DNA. In this issue of Cell, Kumagai et al. (2006) shed light on the molecular mechanism that controls ATR. They report that a physical interaction between ATR and a distinct domain of TopBP1 greatly enhances ATR kinase activity.

KW - Animals

KW - Ataxia Telangiectasia Mutated Proteins

KW - Carrier Proteins

KW - Cell Cycle Proteins

KW - DNA Repair

KW - DNA-Binding Proteins

KW - Enzyme Activation

KW - Gene Expression Regulation

KW - Humans

KW - Models, Genetic

KW - Nuclear Proteins

KW - Protein-Serine-Threonine Kinases

KW - Xenopus Proteins

U2 - 10.1016/j.cell.2006.02.029

DO - 10.1016/j.cell.2006.02.029

M3 - Comment/debate

C2 - 16530035

VL - 124

SP - 888

EP - 890

JO - Cell

JF - Cell

SN - 0092-8674

IS - 5

ER -

ID: 124903417