To spread or not to spread - chromatin modifications in response to DNA damage

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To spread or not to spread - chromatin modifications in response to DNA damage. / Altmeyer, M.; Lukas, J.

In: Current Opinion in Genetics & Development, Vol. 23, No. 2, 09.01.2013, p. 156-165.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Altmeyer, M & Lukas, J 2013, 'To spread or not to spread - chromatin modifications in response to DNA damage', Current Opinion in Genetics & Development, vol. 23, no. 2, pp. 156-165. https://doi.org/10.1016/j.gde.2012.11.001

APA

Altmeyer, M., & Lukas, J. (2013). To spread or not to spread - chromatin modifications in response to DNA damage. Current Opinion in Genetics & Development, 23(2), 156-165. https://doi.org/10.1016/j.gde.2012.11.001

Vancouver

Altmeyer M, Lukas J. To spread or not to spread - chromatin modifications in response to DNA damage. Current Opinion in Genetics & Development. 2013 Jan 9;23(2):156-165. https://doi.org/10.1016/j.gde.2012.11.001

Author

Altmeyer, M. ; Lukas, J. / To spread or not to spread - chromatin modifications in response to DNA damage. In: Current Opinion in Genetics & Development. 2013 ; Vol. 23, No. 2. pp. 156-165.

Bibtex

@article{0982acdc95e44f639076ed2834942b6d,
title = "To spread or not to spread - chromatin modifications in response to DNA damage",
abstract = "Chromatin modifications in response to DNA damage are vital for genome integrity. Multiple proteins and pathways required to generate specialized chromatin domains around DNA lesions have been identified and the increasing amount of information calls for unifying concepts that would allow us to grasp the ever-increasing complexity. This review aims at contributing to this trend by focusing on feed-forward and feedback mechanisms, which in mammalian cells determine the extent of chromatin modifications after DNA damage. We highlight the emerging notion that the nodal points of these highly dynamic pathways operate in a rate-limiting mode, whose deregulation can disrupt physiological boundaries between damaged and undamaged chromatin, dictate repair pathway choice, and determine the fate of cells exposed to genotoxic stress.",
author = "M. Altmeyer and J. Lukas",
year = "2013",
month = jan,
day = "9",
doi = "10.1016/j.gde.2012.11.001",
language = "English",
volume = "23",
pages = "156--165",
journal = "Current Opinion in Genetics & Development",
issn = "0959-437X",
publisher = "Elsevier Ltd. * Current Opinion Journals",
number = "2",

}

RIS

TY - JOUR

T1 - To spread or not to spread - chromatin modifications in response to DNA damage

AU - Altmeyer, M.

AU - Lukas, J.

PY - 2013/1/9

Y1 - 2013/1/9

N2 - Chromatin modifications in response to DNA damage are vital for genome integrity. Multiple proteins and pathways required to generate specialized chromatin domains around DNA lesions have been identified and the increasing amount of information calls for unifying concepts that would allow us to grasp the ever-increasing complexity. This review aims at contributing to this trend by focusing on feed-forward and feedback mechanisms, which in mammalian cells determine the extent of chromatin modifications after DNA damage. We highlight the emerging notion that the nodal points of these highly dynamic pathways operate in a rate-limiting mode, whose deregulation can disrupt physiological boundaries between damaged and undamaged chromatin, dictate repair pathway choice, and determine the fate of cells exposed to genotoxic stress.

AB - Chromatin modifications in response to DNA damage are vital for genome integrity. Multiple proteins and pathways required to generate specialized chromatin domains around DNA lesions have been identified and the increasing amount of information calls for unifying concepts that would allow us to grasp the ever-increasing complexity. This review aims at contributing to this trend by focusing on feed-forward and feedback mechanisms, which in mammalian cells determine the extent of chromatin modifications after DNA damage. We highlight the emerging notion that the nodal points of these highly dynamic pathways operate in a rate-limiting mode, whose deregulation can disrupt physiological boundaries between damaged and undamaged chromatin, dictate repair pathway choice, and determine the fate of cells exposed to genotoxic stress.

UR - http://www.scopus.com/inward/record.url?scp=84877803084&partnerID=8YFLogxK

U2 - 10.1016/j.gde.2012.11.001

DO - 10.1016/j.gde.2012.11.001

M3 - Journal article

C2 - 23312207

AN - SCOPUS:84877803084

VL - 23

SP - 156

EP - 165

JO - Current Opinion in Genetics & Development

JF - Current Opinion in Genetics & Development

SN - 0959-437X

IS - 2

ER -

ID: 46438868