Fig. 1: ZIP13 overexpression caused iron redistribution.
From: Mammalian SLC39A13 promotes ER/Golgi iron transport and iron homeostasis in multiple compartments
a Cytosolic labile iron pool (LIP) in mouse embryonic fibroblasts (MEFs) indicated by Calcein-AM fluorescence (n = 3, biologically independent replicates). Ferrous iron quenches Calcein-AM fluorescence. LIP is indicated by fluorescence difference before and after deferiprone (DFP) treatment. b Cytosolic LIP and Golgi iron in MEFs indicated by Calcein-AM (green) and FeRhonoxTM-1 (magenta), respectively. Stronger fluorescence of Calcein-AM means reduced ferrous iron level. Golgi was marked by P58-GFP (green). Scale bar, 50 μm (Calcein-AM) or 20 μm (FeRhonoxTM-1). c Protein levels of IRP1, IRP2, TfR1, FPN1, FtH, FtL, hZIP13-HA, and dZIP13-MYC determined by immunoblotting. d The mRNA level of Fpn1 was indicated by RT-qPCR (n = 4, biologically independent replicates). e A representative graph of in-gel assays of mitochondrial (m-Aco, encoded by Aconitase2, Aco2) and cytosolic (c-Aco, encoded by Irp1) aconitase in MEFs. f Immunofluorescence colocalization of exogenous hZIP13 (magenta) and Golgi marker P58 (green) in MEFs. DAPI: blue. Scale bar, 20 μm. g Levels of Golgi iron indicated by FeRhonoxTM-1 fluorescence (n = 3, biologically independent replicates). Each experiment at least was repeated independently three times with similar results (c–e). Data are mean ± SD. Statistical analysis was performed using two-tailed student’s t-test (a–g). Source data are provided as a Source Data file.
