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. Author manuscript; available in PMC: 2018 Nov 14.
Published in final edited form as: Toxicol Appl Pharmacol. 2018 Mar 2;344:74. doi: 10.1016/j.taap.2018.03.001

Corrigendum to “Convergence of hepcidin deficiency, systemic iron overloading, heme accumulation, and REV-ERBα/β activation in aryl hydrocarbon receptor-elicited hepatotoxicity” [Toxicol. Appl. Pharmacol. 321 (2017) 1–17]

KA Fader a,b, R Nault a,b, MP Kirby a, G Markous a, J Matthews c, TR Zacharewski a,b,*
PMCID: PMC6235142  NIHMSID: NIHMS993908  PMID: 29501526

After publication of this manuscript, the authors were notified by Abcam that the antibody used to quantify hepatic protein levels of iron responsive element (IRE)-binding protein 2 (IREB2; ab181153) was determined to detect not only IREB2 as marketed, but also aconitase 1 (ACO1; aka IREB1). As a result, Fig. 4B depicts total hepatic levels of both IRE-binding proteins (ACO1 and IREB2) rather than IREB2 specifically. However, both ACO1 and IREB2 regulate transcription/translation of IRE-containing genes through the same mechanism. Therefore, this does not significantly impact our conclusions regarding the effect of TCDD on IRE-binding proteins or overall dysregulation of intracellular iron homeostasis.

The authors would like to apologise for any inconvenience caused.

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