Amyloid Precursor-Like Protein 2 Increases the Endocytosis, Instability, and Turnover of the H2-Kd MHC Class I Molecule
Amyloid Precursor-Like Protein 2 Increases the Endocytosis, Instability, and Turnover of the H2-Kd MHC Class I Molecule
Abstract The defense against the invasion of viruses and tumors relies on the presentation of viral and tumor-derived peptides to CTL by cell surface MHC class I molecules. Previously, we showed that the ubiquitously expressed protein amyloid precursor-like protein 2 (APLP2) associates with the folded form of the MHC class I molecule Kd. In the current study, APLP2 was found to associate with folded Kd molecules following their endocytosis and to increase the amount of endocytosed Kd. In addition, increased expression of APLP2 was shown to decrease Kd surface expression and thermostability. Correspondingly, Kd thermostability and surface expression were increased by down-regulation of APLP2 expression. Overall, these data suggest that APLP2 modulates the stability and endocytosis of Kd molecules.
Protein Folding, Cell Membrane, H-2 Antigens, Temperature, Nerve Tissue Proteins, Endosomes, Endocytosis, Amyloid beta-Protein Precursor, Mice, Gene Expression Regulation, Animals, Humans, HeLa Cells
Protein Folding, Cell Membrane, H-2 Antigens, Temperature, Nerve Tissue Proteins, Endosomes, Endocytosis, Amyloid beta-Protein Precursor, Mice, Gene Expression Regulation, Animals, Humans, HeLa Cells
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