Human ferritin light chain (FTL) mRNA translation is regulated via its 5'-untranslated region (5'-UTR) by three mechanisms: RNA folding, iron response protein binding, and eukaryotic translation initiation factor eIF3 binding.
Heme accumulation is toxic, but deficiency of the heme transporter HRG1/SLC48A1 causes heme sequestration and crystallization into hemozoin within enlarged lysosomes of macrophages, thereby conferring heme tolerance to mammals.
The proteins Bax and Bak, which increase the permeability of the mitochondrial membrane during apoptosis, are also crucial for generating a mitochondrial membrane pore that is specifically involved in necrosis.
Impaired lysosomal acidification results in retention of iron inside lysosomes, triggering functional iron deficiency, dysfunctional mitochondria (especially mtDNA loss), and inflammation in vivo in a mouse model of lysosomal disease.
Conformational changes occur within extracellular domain of BCR upon antigen engagement, and these conformational changes are related with the strength of BCR activation and are distinct in IgM- and IgG-BCR.