Abstract
The FEBS JournalVolume 277, Issue 15 p. 3264-3264 Free Access Corrigendum This article corrects the following: Glycogen synthase kinase 3β and β-catenin pathway is involved in toll-like receptor 4-mediated NADPH oxidase 1 expression in macrophages Jin-Sik Kim, Seungeun Yeo, Dong-Gu Shin, Yoe-Sik Bae, Jae-Jin Lee, Byung-Rho Chin, Chu-Hee Lee, Suk-Hwan Baek, Volume 277Issue 13The FEBS Journal pages: 2830-2837 First Published online: June 1, 2010 First published: 15 July 2010 https://doi.org/10.1111/j.1742-4658.2010.07746.xAboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat The paper by J-S Kim et al. [1] contains an error on page 2830: ‘3 Department of Biochemistry, Dong-A University, Busan, Korea’ should read ‘3 Department of Biological Sciences, School of Natural Sciences, Sungkyunkwan University, Suwon, Korea’. The authors wish to apologize for this error. Reference 1 Kim J-S, Yeo S, Shin D-G, Bae Y-S, Lee J-J, Chin B-R, Lee C-H & Baek S-H (2010) Glycogen synthase kinase 3β and β-catenin pathway is involved in toll-like receptor 4-mediated NADPH oxidase 1 expression in macrophages. FEBS J 277, 2830– 2837. Volume277, Issue15August 2010Pages 3264-3264 ReferencesRelatedInformation
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
