The image in Figure 5d of this Article was inadvertently duplicated from panel e. The correct version of the figure appears below.
(a) Expression of endogenous CNPY3 and gp96 by Raw264.7 after transduction with empty vector (EV), and one or two rounds of gp96 shRNA lentivector. β-Actin is shown as a loading control. (b) Lack of cleaved form of TLR9 (TLR9 m) in the absence of gp96 or CNPY3. Total lysates of wild-type (WT) Raw264.7, cells that were knocked down (KD) for gp96 (gp96 KD) or CNPY3 (CNPY3 KD) were untreated, or treated with Endo H or PNGase F, followed by IB for TLR9HA. (c) WT or gp96 Mut pre-B cells were immunoblotted for TLR9-HA, gp96, CNPY3-FLAG and β-actin. (d) IP of CNPY3 from WT or gp96 KO cells, followed by IB for indicated proteins. (e) IP of TLR9-HA from WT or gp96 KO cells, followed by IB for indicated proteins. ISO indicated IP with isotype control antibody. Two experiments were conducted with similar results.
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The online version of the original article can be found at 10.1038/ncomms1070
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Liu, B., Yang, Y., Qiu, Z. et al. Erratum: Folding of Toll-like receptors by the HSP90 paralogue gp96 requires a substrate-specific cochaperone. Nat Commun 3, 653 (2012). https://doi.org/10.1038/ncomms1398
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DOI: https://doi.org/10.1038/ncomms1398
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