More Modifiers Move on DNA Damage

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More Modifiers Move on DNA Damage. / Morris, Jo.

In: Cancer Research, Vol. 70, No. 10, 15.05.2010, p. 3861-3863.

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Morris, Jo. / More Modifiers Move on DNA Damage. In: Cancer Research. 2010 ; Vol. 70, No. 10. pp. 3861-3863.

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@article{43c11a580cc14c0a856318f42bc663fb,
title = "More Modifiers Move on DNA Damage",
abstract = "In mammalian cells the accumulation of repair proteins to double-strand breaks is a phosphorylation- and ubiquitylation-regulated process. Some of the genes that encode the kinases and ubiquitin ligases in this pathway are cancer predisposition genes, most prominently the breast cancer predisposition gene BRCA1, which encodes a ubiquitin ligase. How BRCA1 ligase activity was regulated following DNA damage was poorly understood. In this review I summarize new data that show a third post-translational modification, by the small ubiquitin like modifier SUMO, is part of the same cascade, enabling and activating DNA damage-regulated processes, including the BRCA1 ligase activity.",
author = "Jo Morris",
year = "2010",
month = may,
day = "15",
doi = "10.1158/0008-5472.CAN-10-0468",
language = "English",
volume = "70",
pages = "3861--3863",
journal = "Cancer Research",
issn = "0008-5472",
publisher = "American Association for Cancer Research",
number = "10",

}

RIS

TY - JOUR

T1 - More Modifiers Move on DNA Damage

AU - Morris, Jo

PY - 2010/5/15

Y1 - 2010/5/15

N2 - In mammalian cells the accumulation of repair proteins to double-strand breaks is a phosphorylation- and ubiquitylation-regulated process. Some of the genes that encode the kinases and ubiquitin ligases in this pathway are cancer predisposition genes, most prominently the breast cancer predisposition gene BRCA1, which encodes a ubiquitin ligase. How BRCA1 ligase activity was regulated following DNA damage was poorly understood. In this review I summarize new data that show a third post-translational modification, by the small ubiquitin like modifier SUMO, is part of the same cascade, enabling and activating DNA damage-regulated processes, including the BRCA1 ligase activity.

AB - In mammalian cells the accumulation of repair proteins to double-strand breaks is a phosphorylation- and ubiquitylation-regulated process. Some of the genes that encode the kinases and ubiquitin ligases in this pathway are cancer predisposition genes, most prominently the breast cancer predisposition gene BRCA1, which encodes a ubiquitin ligase. How BRCA1 ligase activity was regulated following DNA damage was poorly understood. In this review I summarize new data that show a third post-translational modification, by the small ubiquitin like modifier SUMO, is part of the same cascade, enabling and activating DNA damage-regulated processes, including the BRCA1 ligase activity.

U2 - 10.1158/0008-5472.CAN-10-0468

DO - 10.1158/0008-5472.CAN-10-0468

M3 - Article

C2 - 20406985

VL - 70

SP - 3861

EP - 3863

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 10

ER -