SEC61A1 and autosomal dominant medullary cystic kidney disease with or without hyperuricemia: Other soluble (preproapelin and preprocecropin) and membrane-integrated (cytochrome b5 and Sec61β) substrates tested under post-translational transport conditions, that is, SPCs are added after protein synthesis is fully completed, were not affected by the ADTKD–SEC61A1 mutations (Figs 3C and D and S4G).