-
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.
-
modification of Tapasin can enhance the presentation of targeting antigens via intracellular delivery to DCs and elicit specific CTL immune responses efficiently
-
Data show that tapasin expression is enhanced by beta 2-microglobulin via both transcriptional and post-transcriptional mechanisms.
-
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).
-
E2F1 is an essential transcription factor for tapasin.
-
showed that a large disulfide-bonded complex was present in the mouse cells that included ERp57, tapasin, and K(d).
-
Role of tapasin in MHC class I antigen presentation in vivo.
-
Data show that cell surface expression of TAP-independent class I complexes is modulated by tapasin levels and is enhanced by interferon-gamma.
-
tapasin has a essential function of tapasin in quality control of HLA-G molecules
-
A major role for tapasin as a stabilizer of the TAP peptide transporter and consequences for MHC class I expression.
-
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.
-
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.
-
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.
-
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.
-
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.
-
Essential for stable expression of the antigen-processing transmembrane domain of the TAP2 protein.
-
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.
-
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.
-
Tapasin editing is a contributing factor to the phenomenon of immunodominance.
-
During the assembly of H2-M3, tapasin directly facilitates intracellular peptide binding but is not required for intracellular retention of open conformers.
