BPG is committed to discovery and dissemination of knowledge
Articles Published Processes
5/30/2015 1:35:00 PM | Browse: 1352 | Download: 2968
 |
Received |
|
2014-10-13 08:48 |
 |
Peer-Review Started |
|
2014-10-13 20:47 |
 |
First Decision by Editorial Office Director |
|
|
 |
Return for Revision |
|
2014-11-20 09:14 |
 |
Revised |
|
2014-12-12 15:16 |
 |
Publication Fee Transferred |
|
|
 |
Second Decision by Editor |
|
2015-02-04 08:04 |
 |
Second Decision by Editor-in-Chief |
|
2015-02-04 08:24 |
 |
Final Decision by Editorial Office Director |
|
2015-02-12 21:18 |
 |
Articles in Press |
|
2015-02-13 11:23 |
 |
Edit the Manuscript by Language Editor |
|
2015-03-05 10:41 |
 |
Typeset the Manuscript |
|
2015-05-13 17:31 |
 |
Publish the Manuscript Online |
|
2015-05-30 13:32 |
| ISSN |
1007-9327 (print) and 2219-2840 (online) |
| Open Access |
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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/ |
| Copyright |
© The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
|
| Article Reprints |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/247
|
| Permissions |
For details, please visit: http://www.wjgnet.com/bpg/gerinfo/207
|
| Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
| Website |
http://www.wjgnet.com |
| Category |
Gastroenterology & Hepatology |
| Manuscript Type |
Basic Study |
| Article Title |
SGK1 inhibits cellular apoptosis and promotes proliferation via the MEK/ERK/p53 pathway in colitis
|
| Manuscript Source |
Unsolicited Manuscript |
| All Author List |
Jian-An Bai, Gui-Fang Xu, Li-Jun Yan, Wei-Wen Zeng, Qian-Qian Ji, Jin-Dao Wu and Qi-Yun Tang |
| Funding Agency and Grant Number |
| Funding Agency |
Grant Number |
| National Natural Science Foundation of China |
81470806 |
| National Natural Science Foundation of Jiangsu Province |
BK20141496 |
| Public Health Ministry of Jiangsu Province in the Talents in Medical Science Program |
RC201179 |
|
| Corresponding Author |
Qi-Yun Tang, MD, PhD, Department of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Rd, Nanjing 210029, China. tqy831@163.com |
| Key Words |
Colitis; Serum-and-glucocorticoid-inducible-kinase-1; MEK/ERK; Apoptosis; p53 |
| Core Tip |
This study showed that serum-and-glucocorticoid-inducible-kinase-1 (SGK1) expression was significantly increased in the inflamed epithelia of patients with active Crohn’s disease (CD) in a TNBS-induced colitis model. At the cellular level, silencing of SGK1 inhibited the phosphorylation of mitogen-activated protein kinase kinase 1 (MEK1) and the downstream molecule ERK1/2, which induced the upregulation of p53 and Bcl-2-associated X protein, triggering subsequent cellular apoptosis and inhibition of proliferation in intestinal epithelial cells. A MEK1 inhibitor (i.e., U0126) was used to show that this was a MEK/ERK-dependent process. Co-immunoprecipitation analysis uncovered the mechanism of the interaction between SGK1 and MEK1. Our results provide a new therapeutic approach to CD therapy. |
| Publish Date |
2015-05-30 13:32 |
| Citation |
Bai JA, Xu GF, Yan LJ, Zeng WW, Ji QQ, Wu JD, Tang QY. SGK1 inhibits cellular apoptosis and promotes proliferation via the MEK/ERK/p53 pathway in colitis. World J Gastroenterol 2015; 21(20): 6180-6193 |
| URL |
http://www.wjgnet.com/1007-9327/full/v21/i20/6180.htm |
| DOI |
http://dx.doi.org/10.3748/wjg.v21.i20.6180 |
All content on this site: Copyright © 1993-2026 Baishideng Publishing Group Inc, its licensors, and contributors. All rights are reserved, including those for text and data mining, AI training, and similar technologies. For all open access content, the relevant licensing terms apply.