Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk I

To determine the effects of heme synthesis inhibition via different pathways in erythroid progenitor cells, heme synthesis was inhibited by 50 µM DTPA treatment (a zinc chelator), 50 µM DFO treatment (a iron chelator), or 0.2 mM succinylacetone (SA, a ALAD inhibitor) for 24 hours in differentiating G1E-ER4 cells. G1E-ER4 Cells were divided into four groups: untreated control, 50 µM DTPA treatment, 50 µM DFO treatment, and 0.2 mM SA. The transcriptome profiles acquired from RNA-seq were compared with those of control cells. Overall design: Comparative gene expression profiling of control G1E-ER4 cells and those deficient in cellular zinc, cellular iron, or ALAD activity (n = 3 biological replicates per group)