Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming

ARID1A, which is often mutated in human endometrial cancer, is a component of the SWI/SNF chromatin remodelling complex. Here, the authors show that Arid1a mutations in the mouse endometrium and primary human endometrial epithelial cells cause widespread reprogramming of gene transcription and resul...

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Autores principales: Yohan Suryo Rahmanto, Wenjing Shen, Xu Shi, Xi Chen, Yu Yu, Zheng-Cheng Yu, Tsutomu Miyamoto, Meng-Horng Lee, Vivek Singh, Ryoichi Asaka, Geoffrey Shimberg, Michele I. Vitolo, Stuart S. Martin, Denis Wirtz, Ronny Drapkin, Jianhua Xuan, Tian-Li Wang, Ie-Ming Shih
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Publicado: Nature Portfolio 2020
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Acceso en línea:https://doaj.org/article/75bea59380ee4facabb9a13db669ea7a
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spelling oai:doaj.org-article:75bea59380ee4facabb9a13db669ea7a2021-12-02T17:51:19ZInactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming10.1038/s41467-020-16416-02041-1723https://doaj.org/article/75bea59380ee4facabb9a13db669ea7a2020-06-01T00:00:00Zhttps://doi.org/10.1038/s41467-020-16416-0https://doaj.org/toc/2041-1723ARID1A, which is often mutated in human endometrial cancer, is a component of the SWI/SNF chromatin remodelling complex. Here, the authors show that Arid1a mutations in the mouse endometrium and primary human endometrial epithelial cells cause widespread reprogramming of gene transcription and result in a loss of response to TGFβ.Yohan Suryo RahmantoWenjing ShenXu ShiXi ChenYu YuZheng-Cheng YuTsutomu MiyamotoMeng-Horng LeeVivek SinghRyoichi AsakaGeoffrey ShimbergMichele I. VitoloStuart S. MartinDenis WirtzRonny DrapkinJianhua XuanTian-Li WangIe-Ming ShihNature PortfolioarticleScienceQENNature Communications, Vol 11, Iss 1, Pp 1-14 (2020)
institution DOAJ
collection DOAJ
language EN
topic Science
Q
spellingShingle Science
Q
Yohan Suryo Rahmanto
Wenjing Shen
Xu Shi
Xi Chen
Yu Yu
Zheng-Cheng Yu
Tsutomu Miyamoto
Meng-Horng Lee
Vivek Singh
Ryoichi Asaka
Geoffrey Shimberg
Michele I. Vitolo
Stuart S. Martin
Denis Wirtz
Ronny Drapkin
Jianhua Xuan
Tian-Li Wang
Ie-Ming Shih
Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming
description ARID1A, which is often mutated in human endometrial cancer, is a component of the SWI/SNF chromatin remodelling complex. Here, the authors show that Arid1a mutations in the mouse endometrium and primary human endometrial epithelial cells cause widespread reprogramming of gene transcription and result in a loss of response to TGFβ.
format article
author Yohan Suryo Rahmanto
Wenjing Shen
Xu Shi
Xi Chen
Yu Yu
Zheng-Cheng Yu
Tsutomu Miyamoto
Meng-Horng Lee
Vivek Singh
Ryoichi Asaka
Geoffrey Shimberg
Michele I. Vitolo
Stuart S. Martin
Denis Wirtz
Ronny Drapkin
Jianhua Xuan
Tian-Li Wang
Ie-Ming Shih
author_facet Yohan Suryo Rahmanto
Wenjing Shen
Xu Shi
Xi Chen
Yu Yu
Zheng-Cheng Yu
Tsutomu Miyamoto
Meng-Horng Lee
Vivek Singh
Ryoichi Asaka
Geoffrey Shimberg
Michele I. Vitolo
Stuart S. Martin
Denis Wirtz
Ronny Drapkin
Jianhua Xuan
Tian-Li Wang
Ie-Ming Shih
author_sort Yohan Suryo Rahmanto
title Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming
title_short Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming
title_full Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming
title_fullStr Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming
title_full_unstemmed Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming
title_sort inactivation of arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming
publisher Nature Portfolio
publishDate 2020
url https://doaj.org/article/75bea59380ee4facabb9a13db669ea7a
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