Fig. 6: Characterization of proteasome subunit missense variants. | Nature Communications

Fig. 6: Characterization of proteasome subunit missense variants.

From: Heterozygous missense variant of the proteasome subunit β-type 9 causes neonatal-onset autoinflammation and immunodeficiency

Fig. 6

a Locational distribution of published missense variant sites on the schematic model of β rings in the immunoproteasome (https://infevers.umai-montpellier.fr/web/index.php). The mutant residues are represented by red circles. Catalytic active sites in β1i, β2i, and β5i are marked with orange circles. Notably, PSMB9 G156 and PSMB10 G209 are at the interface of two β rings, while most of mutated residues in PSMB8 are at or around active sites. b Multiple alignments of PSMB10 (β2i) and PSMB2 (β2) in various species. Conserved amino acids among all these species are indicated by asterisks. G209 in murine PSMB10 and the corresponding amino acids are indicated in red. c The structure model of wildtype and PSMB10 G209W mutant of the 20S complex, based on the β2i-subunit structure [Protein Data Bank (PDB) ID code 3UNH]. The overall structure of the 20S complex is shown as a ribbon model. β2i and β6 subunits are shown as light blue and orange, respectively. W209 and some of the potential interacting residues of PSMB10 G209W mutant are shown in stick representation.

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