Mutually exclusive amino acid residues of L13a are responsible for its ribosomal incorporation and translational silencing leading to resolution of inflammation

Nuclear and nucleolar localization of L13a variants lacking predicted NLSs or residues important for translational silencing. Nuclear and nucleolar localization of additional L13a variants (1–84 + 119–203; predicted NLS1 deleted), (1–84 + 119–148; predicted NLS1 and NLS2 deleted), and K169A–K170A–K171A (translational silencing incompetent, see Fig. 7) was analyzed by immunofluorescence as described in Figure 4.