Correction to: Nature Communications https://doi.org/10.1038/s41467-020-14809-9, published online 25 February 2020.
In the original version of this Article, previous work by Calzoni et al.51 was inadvertently misrepresented in the penultimate paragraph of the Discussion. It incorrectly read ‘Very recently, Calzoni et al. published a short letter and reported biallelic mutations in FCHO1 in four families. The phenotypes of these patients resembled the phenotype of our patients, but no functional experiments or proof-of-causality was provided. Based on experiments in activated T-cell blasts, the authors concluded that in the absence of FCHO1, CME is globally affected. In contrast, our data support the concept that FCHO1 does not globally affect CME51.’
The correct version states ‘While our study was under review, Calzoni et al. reported biallelic mutations in FCHO1 in four families51. The phenotypes of these patients resembled the phenotype of our patients. Based on experiments in activated T-cell blasts, the authors concluded that in the absence of FCHO1, CME of the transferrin receptor is affected51. In contrast, our data support the concept that FCHO1 does not control internalization of the transferrin receptor and mediates more subtle effects on CME.’
This has been corrected in both the PDF and HTML versions of the Article.
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Łyszkiewicz, M., Ziętara, N., Frey, L. et al. Author Correction: Human FCHO1 deficiency reveals role for clathrin-mediated endocytosis in development and function of T cells. Nat Commun 11, 1963 (2020). https://doi.org/10.1038/s41467-020-15946-x
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DOI: https://doi.org/10.1038/s41467-020-15946-x
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