Nature Communications 8:790 10.1038/s41467-017-00797-w; Article published online: 5 October 2017
Previous work by Garcia Ponce et al. and Citalán-Madrid et al. suggesting a link between cortactin and RhoA-mediated actomyosin contractility was inadvertently omitted from the original version of this manuscript and should have been cited within the “Discussion” section as follows:
“Previous studies in cortactin-null endothelium and intestinal epithelium revealed hyperactivated RhoA-mediated contractility in these cell types, contrasting with the decrease in junctional RhoA signaling and contractility that we observed, but the direct involvement of cortactin in mediating actomyosin contractility was not established1,2. Future research will have to explore the compatibility of these observations.”
1. Garcia Ponce, A. et al. Loss of cortactin causes endothelial barrier dysfunction via disturbed adrenomedullin secretion and actomyosin contractility. Sci Rep. 6, 29003 (2016).
2. Citalán-Madrid, A. F. et al. Cortactin deficiency causes increased RhoA/ROCK1-dependent actomyosin contractility, intestinal epithelial barrier dysfunction, and disproportionately severe DSS-induced colitis. Mucosal Immunol. 10, 1237–1247 (2017).
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The original article can be found online at https://doi.org/10.1038/s41467-017-00797-w.
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Liang, X., Budnar, S., Gupta, S. et al. Author Correction: Tyrosine dephosphorylated cortactin downregulates contractility at the epithelial zonula adherens through SRGAP1. Nat Commun 8, 2021 (2017). https://doi.org/10.1038/s41467-017-02131-w
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DOI: https://doi.org/10.1038/s41467-017-02131-w
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