Corrigendum to “Disruption of the potassium channel regulatory subunit KCNE2 causes iron-deficient anemia” [Experimental Hematology, Vol. 42, Issue 12, p1053–1058.e1

Abstract

The authors regret that an incorrect reference was cited in the discussion section. “Interestingly, these findings could be clinically relevant, as it was recently reported that impaired function of KCNQ1 in Jervell and Lange-Nielsen syndrome results in iron-deficient anemia and gastric hyperplasia [15].” The cited number 15 reference is wrongly listed as Grove et al 2010 and should instead be Iron-deficiency anaemia, gastric hyperplasia, and elevated gastrin levels due to potassium channel dysfunction in the Jervell and Lange-Nielsen Syndrome. Winbo A, Sandström O, Palmqvist R, Rydberg A. Cardiol Young. 2013 Jun;23(3):325-34. The authors would like to apologise for any inconvenience caused. Disruption of the potassium channel regulatory subunit KCNE2 causes iron-deficient anemiaExperimental HematologyVol. 42Issue 12PreviewIron homeostasis is a dynamic process that is tightly controlled to balance iron uptake, storage, and export. Reduction of dietary iron from the ferric to the ferrous form is required for uptake by solute carrier family 11 (proton-coupled divalent metal ion transporters), member 2 (Slc11a2) into the enterocytes. Both processes are proton dependent and have led to the suggestion of the importance of acidic gastric pH for the absorption of dietary iron. Potassium voltage-gated channel subfamily E, member 2 (KCNE2), in combination with potassium voltage-gated channel, KQT-like subfamily, member 1 (KCNQ1), form a gastric potassium channel essential for gastric acidification. Full-Text PDF Open Access