LIG4 mediates Wnt signalling-induced radioresistance
The Wnt/β-catenin signalling pathway contributes to radio resistance in intestinal stem cells but the underlying mechanism is currently unknown. In this study, the authors demonstrate that LIG4, a DNA ligase involved in the DNA repair process, is a direct target of β-catenin and it specifically medi...
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2016-03-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/ncomms10994 |
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doaj-581765a279824025a9bb4b79da323deb2021-05-11T11:20:40ZengNature Publishing GroupNature Communications2041-17232016-03-017111310.1038/ncomms10994LIG4 mediates Wnt signalling-induced radioresistanceSohee Jun0Youn-Sang Jung1Han Na Suh2Wenqi Wang3Moon Jong Kim4Young Sun Oh5Esther M. Lien6Xi Shen7Yoshihisa Matsumoto8Pierre D. McCrea9Lei Li10Junjie Chen11Jae-Il Park12Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterResearch Laboratory for Nuclear Reactors, Tokyo Institute of TechnologyDepartment of Molecular Genetics, The University of Texas MD Anderson Cancer CenterDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterDepartment of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer CenterThe Wnt/β-catenin signalling pathway contributes to radio resistance in intestinal stem cells but the underlying mechanism is currently unknown. In this study, the authors demonstrate that LIG4, a DNA ligase involved in the DNA repair process, is a direct target of β-catenin and it specifically mediates non-homologous end joining repair in colorectal cancer cells.https://doi.org/10.1038/ncomms10994 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Sohee Jun Youn-Sang Jung Han Na Suh Wenqi Wang Moon Jong Kim Young Sun Oh Esther M. Lien Xi Shen Yoshihisa Matsumoto Pierre D. McCrea Lei Li Junjie Chen Jae-Il Park |
spellingShingle |
Sohee Jun Youn-Sang Jung Han Na Suh Wenqi Wang Moon Jong Kim Young Sun Oh Esther M. Lien Xi Shen Yoshihisa Matsumoto Pierre D. McCrea Lei Li Junjie Chen Jae-Il Park LIG4 mediates Wnt signalling-induced radioresistance Nature Communications |
author_facet |
Sohee Jun Youn-Sang Jung Han Na Suh Wenqi Wang Moon Jong Kim Young Sun Oh Esther M. Lien Xi Shen Yoshihisa Matsumoto Pierre D. McCrea Lei Li Junjie Chen Jae-Il Park |
author_sort |
Sohee Jun |
title |
LIG4 mediates Wnt signalling-induced radioresistance |
title_short |
LIG4 mediates Wnt signalling-induced radioresistance |
title_full |
LIG4 mediates Wnt signalling-induced radioresistance |
title_fullStr |
LIG4 mediates Wnt signalling-induced radioresistance |
title_full_unstemmed |
LIG4 mediates Wnt signalling-induced radioresistance |
title_sort |
lig4 mediates wnt signalling-induced radioresistance |
publisher |
Nature Publishing Group |
series |
Nature Communications |
issn |
2041-1723 |
publishDate |
2016-03-01 |
description |
The Wnt/β-catenin signalling pathway contributes to radio resistance in intestinal stem cells but the underlying mechanism is currently unknown. In this study, the authors demonstrate that LIG4, a DNA ligase involved in the DNA repair process, is a direct target of β-catenin and it specifically mediates non-homologous end joining repair in colorectal cancer cells. |
url |
https://doi.org/10.1038/ncomms10994 |
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