Author Correction | Published:

Author Correction: EphA2 is an epithelial cell pattern recognition receptor for fungal β-glucans

Nature Microbiologyvolume 3page1074 (2018) | Download Citation

Correction to: Nature Microbiology https://doi.org/10.1038/s41564-017-0059-5, published online 13 November 2017.

In the version of this Article originally published, the authors described the ANT compound used in their study as 4-(2,5-dimethyl-1H-pyrrol-1-yl)-2-hydroxybenzoic acid (ANT). The authors now wish to clarify that the ANT compound used was actually a 2,5-dimethylpyrrolyl benzoic acid derivative1 that has been shown to inhibit not only the enzymatic activity of EphA2, but also several unrelated enzymes2. The description of the compound in the Article has now been changed to 4-(2,5-dimethyl-1H-pyrrol-1-yl)-2-hydroxybenzoic acid derivative (ANT) to reflect this.

However, given that the data obtained with ANT in this study were verified by experiments with EphA2 siRNA, recombinant EphA2 and EphA2–/– mice, the conclusions of the study are not affected by the limited specificity of the inhibitor.

References

  1. 1.

    Noberini, R. et al. A disalicylic acid-furanyl derivative inhibits ephrin binding to a subset of Eph receptors. Chem. Biol. Drug. Des. 78, 667–678 (2011).

  2. 2.

    Baell, J. B. & Holloway, G. A. New substructure filters for removal of pan assay interference compounds (PAINS) from screening libraries and for their exclusion in bioassays. J. Med. Chem. 53, 2719–2740 (2010).

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Affiliations

  1. Division of Infectious Diseases, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, USA

    • Marc Swidergall
    • , Norma V. Solis
    •  & Scott G. Filler
  2. National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fungal Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, Bethesda, MD, USA

    • Michail S. Lionakis
  3. David Geffen School of Medicine at UCLA, Los Angeles, CA, USA

    • Scott G. Filler

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Correspondence to Scott G. Filler.

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https://doi.org/10.1038/s41564-018-0188-5