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4/28/2021 8:19:05 AM | Browse: 192 | Download: 319
Publication Name World Journal of Gastroenterology
Manuscript ID 65462
Country China
Category Gastroenterology & Hepatology
Manuscript Type Basic Study
Article Title Enhancer of zeste homolog 2 contributes to apoptosis by inactivating JAK2/STAT signaling in inflammatory bowel disease
Manuscript Source Unsolicited Manuscript
All Author List Jie Zhou, Yang Yang, Yi-Ling Wang, Yue Zhao, Wen-Jing Ye, Si-Yao Deng, Jin-Yi Lang and Shun Lu
Funding Agency and Grant Number
Funding Agency Grant Number
National Natural Science Foundation of China 81900498
Corresponding Author Shun Lu, MD, Chief Physician, Department of Radiation Oncology, Sichuan Cancer Hospital, No. 55 Renmin South Road, Chengdu 610041, Sichuan Province, China. lushousi90036@163.com
Key Words Inflammatory bowel disease; Apoptosis; Enhancer of zeste homolog 2; JAK2; Permeability; Inflammatory bowel disease therapy
Core Tip In this study, we discovered that enhancer of zeste homolog 2 (EZH2) contributed to apoptosis and inflammatory response by inactivating JAK2/STAT signaling in inflammatory bowel disease (IBD). EZH2 may be applied as the potential targets for IBD therapy.
Citation Zhou J, Yang Y, Wang YL, Zhao Y, Ye WJ, Deng SY, Lang JY, Lu S. Enhancer of zeste homolog 2 contributes to apoptosis by inactivating JAK2/STAT signaling in inflammatory bowel disease. World J Gastroenterol 2021; 27(22): 3073-3084
Received
2021-03-07 17:57
Peer-Review Started
2021-03-07 18:01
To Make the First Decision
Return for Revision
2021-03-27 17:50
Revised
2021-04-09 07:41
Second Decision
2021-04-28 07:54
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief
2021-04-28 08:19
Articles in Press
2021-04-28 08:19
Publication Fee Transferred
Edit the Manuscript by Language Editor
2021-05-10 14:32
Typeset the Manuscript
2021-06-03 06:01
ISSN 1007-9327 (print) and 2219-2840 (online)
Open Access This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
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