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Qa-1b-restricted CD8+ T cells display characteristics of both conventional hypervariable T cells as well as invariant T cells and can be classified as semi-invariant T cells, with only conserved Valpha usage, positioned between these two known T cell subsets.
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Absence of Tpn or ERAAP independently altered the peptide repertoire by causing loss as well as gain of new pMHC I. Tpn defined the characteristic carboxy termini of canonical MHC I peptides.
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modification of Tapasin can enhance the presentation of targeting antigens via intracellular delivery to DCs and elicit specific CTL immune responses efficiently
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Data show that tapasin expression is enhanced by beta 2-microglobulin via both transcriptional and post-transcriptional mechanisms.
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Deletion of a loop within the tapasin C-terminal Ig-like domain (Delta334-342) prevented tapasin association with the MHC class I molecule K(d).
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E2F1 is an essential transcription factor for tapasin.
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showed that a large disulfide-bonded complex was present in the mouse cells that included ERp57, tapasin, and K(d).
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Role of tapasin in MHC class I antigen presentation in vivo.
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Data show that cell surface expression of TAP-independent class I complexes is modulated by tapasin levels and is enhanced by interferon-gamma.
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tapasin has a essential function of tapasin in quality control of HLA-G molecules
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A major role for tapasin as a stabilizer of the TAP peptide transporter and consequences for MHC class I expression.
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Tapasin is required for class I major histocompatibility complex (MHC-I) to bind endoplasmic reticulum-derived stabilizing peptides to achieve stability needed for alternate MHC-I processing via peptide exchange in acidic vacuolar processing compartments.
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Mutational analysis of tapasin provides insight into aspects of tapasin structure that are crucial to its ability to assist major histocompatibility complex class I assembly.
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demonstrate a key role for tapasin in shaping the MHC class I peptide repertoire, as enhancement of presentation in the presence of tapasin correlated with peptide half-life.
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Tapasin links class Ib molecule Qa-1b to the transporter associated with antigen processing (TAP) peptide and facilitates the delivery of Qa-1b to the cell surface.
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Mouse tapasin has quantitative and qualitative effects on the HLA-B*2705-bound peptide repertoire, impairing presentation of some suitable ligands and allowing others with suboptimal anchor residues and lower affinity to be presented.
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Essential for stable expression of the antigen-processing transmembrane domain of the TAP2 protein.
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A K408W mutation in the transmembrane/cytoplasmic domain disrupted K(d) folding & release from tapasin, but not interaction with TAP. The C terminus plays a role in enabling class I molecules to be expressed at the surface of mouse cells.
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the free cysteine 95 in mouse tapasin influences stable expression at the plasma membrane for both MHC class I allotypes, and have shown that tapasin's interaction with folded K(d) is elevated by the C95S substitution in tapasin.
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Tapasin editing is a contributing factor to the phenomenon of immunodominance.
