Using primary mouse macrophages, Wang et al. (2007) found that knockdown of Mon1a with small interfering RNA (siRNA) led to the intracellular accumulation of ferroportin (SLC40A1; 604653) and the absence of ferroportin at the cell surface. Knockdown of Mon1a had no effect on iron loading, but inhibited iron release. Inhibition of Mon1a also prevented lipopolysaccharide (LPS)-induced expression of MHC class II molecules on the cell surface and the secretion of interleukin-6 (IL6; 147620) and Il12 (see 161560). Knockdown of mouse Mon1a interrupted trafficking through the secretory apparatus without affecting endocytic trafficking to lysosomes or the size and distribution of lysosomes.