Abstract
The Journal of PhysiologyVolume 590, Issue 6 p. 1511-1511 Free Access Corrigenda This article corrects the following: Epac2-dependent mobilization of intracellular Ca2+ by glucagon-like peptide-1 receptor agonist exendin-4 is disrupted in β-cells of phospholipase C-ɛ knockout mice Igor Dzhura, Oleg G. Chepurny, Grant G. Kelley, Colin A. Leech, Michael W. Roe, Elvira Dzhura, Parisa Afshari, Sundeep Malik, Michael J. Rindler, Xin Xu, Youming Lu, Alan V. Smrcka, George G. Holz, Volume 588Issue 24The Journal of Physiology pages: 4871-4889 First Published online: December 15, 2010 First published: 30 January 2012 https://doi.org/10.1113/jphysiol.2012.228312AboutSectionsPDF 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 In the article by Dzhura et al. (2010) there was an error in the Methods section entitled ‘Generation of Epac2 knockout mice’ on page 4873. The first sentence of that section should read ‘Epac2 KO mice with global disruption of RAPGEF4 gene expression (NCBI GeneID 56508) were generated by the Texas A&M Institute for Genomic Medicine through customized service for Dr. Lu at Louisiana State University Health Sciences Center.’ References Dzhura I, Chepurny OG, Kelley GG, Leech CA, Roe MW, Dzhura E, Afshari P, Malik S, Rindler MJ, Xu X, Lu Y, Smrcka AV & Holz GG (2010). Epac2-dependent mobilization of intracellular Ca2+ by glucagonlike peptide-1 receptor agonist exendin-4 is disrupted in β-cells of phospholipase C-ɛ knockout mice. J Physiol 588, 4871– 4889. Volume590, Issue6March 2012Pages 1511-1511 ReferencesRelatedInformation
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: 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.