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12/10/2014 3:50:00 PM | Browse: 797 | Download: 805
Publication Name World Journal of Gastroenterology
Manuscript ID 11644
Country Germany
Received
2014-05-29 09:32
Peer-Review Started
2014-05-29 23:30
To Make the First Decision
2014-06-18 17:19
Return for Revision
2014-06-23 09:32
Revised
2014-06-30 21:24
Second Decision
2014-08-28 09:56
Accepted by Journal Editor-in-Chief
Accepted by Company Editor-in-Chief
2014-08-28 10:12
Articles in Press
2014-08-28 10:51
Publication Fee Transferred
Edit the Manuscript by Language Editor
Typeset the Manuscript
2014-11-26 20:28
Publish the Manuscript Online
2014-12-10 15:52
ISSN 1007-9327 (print) and 2219-2840 (online)
Open Access
Copyright
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 Cell Biology
Manuscript Type Autobiography
Article Title CYLD deletion triggers nuclear factor-kB-signaling and increases cell death resistance in murine hepatocytes
Manuscript Source Unsolicited Manuscript
All Author List Toni Urbanik, Bruno Christian Koehler, Laura Wolpert, Christin Elßner, Anna-Lena Scherr, Thomas Longerich, Nicole Kautz, Stefan Welte, Nadine Hövelmeyer, Dirk Jäger, Ari Waisman and Henning Schulze-Bergkamen
Funding Agency and Grant Number
Funding Agency Grant Number
Dietmar Hopp Stiftung, http://www.dietmar-hopp-stiftung.de
German Research Foundation (Deutsche Forschungsgemeinschaft) DFG SCHU 1443/3-2 (to HSB)
German Research Foundation (Deutsche Forschungsgemeinschaft) SFB/TRR 77
Corresponding Author Henning Schulze-Bergkamen, MD, National Center for Tumor Diseases, Department of Medical Oncology, University Clinic of Heidelberg, Im Neuenheimer Feld 460, 69120 Heidelberg, Baden-Wuerrtemberg, Germany. henning.schulze@med.uni-heidelberg.de
Key Words CYLD; Apoptosis; Nuclear factor-B; Tumor necrosis factor-; CD95; Liver
Core Tip Activation of death receptors, such as CD95 (Fas/APO-1) and tumor necrosis factor (TNF)-R1, is involved in the pathophysiology of acute and chronic liver diseases. Inactivation of the deubiquitinase CYLD is accompanied by increased survival of different cell types. However, the role of CYLD in death receptor-mediated apoptosis of hepatocytes has not been addressed so far. The study showed for the first time that CYLD negative hepatocytes are less sensitive to CD95 and TNF-R-mediated apoptosis, at least in part via triggering nuclear factor-?B signaling leading to induction of anti-apoptotic proteins. Inhibition of CYLD might represent a therapeutic approach to protect hepatocytes from death receptor-mediated apoptosis.
Publish Date 2014-12-10 15:52
Citation Urbanik T, Koehler BC, Wolpert L, Elßner C, Scherr AL, Longerich T, Kautz N, Welte S, Hövelmeyer N, Jäger D, Waisman A, Schulze-Bergkamen H. CYLD deletion triggers nuclear factor-B-signaling and increases cell death resistance in murine hepatocytes. World J Gastroenterol 2014; 20(45): 17049-1706
URL http://www.wjgnet.com/1007-9327/full/v20/i45/17049.htm
DOI http://dx.doi.org/10.3748/wjg.v20.i45.17049
Full Article (PDF) WJG-20-17049.pdf
Full Article (Word) WJG-20-17049.doc
Manuscript File 11644-Reveiw.docx
Answering Reviewers 11644-Answering reviewers.pdf
Copyright License Agreement 11644-Copyright assignment.pdf
Peer-review Report 11644-Peer review(s).pdf
Scientific Misconduct Check 11644-CrossCheck.jpg
Scientific Editor Work List 11644-Scientific editor work list.pdf