Correction: Tyrosine dephosphorylated cortactin downregulates contractility at the epithelial zonula adherens through SRGAP1 author-correction (Nature Communications (2017)8 (790) DOI: 10.1038/s41467-017-00797-w)

Xuan Liang, Srikanth Budnar, Shafali Gupta, Suzie Verma, Siew Ping Han, Michelle M. Hill, Roger J. Daly, Robert G. Parton, Nicholas A. Hamilton, Guillermo A. Gomez, Alpha S. Yap

Research output: Contribution to journalComment / DebateOtherpeer-review

Abstract

"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 a myosin 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, intestinalepithelial barrier dysfunction, and disproportionately severe DSS-induced colitis. Mucosal Immunol. 10, 1237-1247 (2017). 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).

Original languageEnglish
Article number2021
Number of pages1
JournalNature Communications
Volume8
Issue number1
DOIs
Publication statusPublished - 1 Dec 2017

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