anti-TAP Binding Protein (Tapasin) (TAPBP) Antibodies

Mouse (Murine) TAP Binding Protein (Tapasin) (TAPBP) interaction partners

1. These results combined with mutation analyses allow us to propose a molecular model underlying MHC-I peptide selection by tapasin.

2. 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.

3. 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.

4. modification of Tapasin can enhance the presentation of targeting antigens via intracellular delivery to DCs and elicit specific CTL immune responses efficiently

5. Data show that tapasin expression is enhanced by beta 2-microglobulin via both transcriptional and post-transcriptional mechanisms.

6. 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).

7. E2F1 is an essential transcription factor for tapasin.

8. showed that a large disulfide-bonded complex was present in the mouse cells that included ERp57, tapasin, and K(d).

9. Role of tapasin in MHC class I antigen presentation in vivo.

10. Data show that cell surface expression of TAP-independent class I complexes is modulated by tapasin levels and is enhanced by interferon-gamma.

11. tapasin has a essential function of tapasin in quality control of HLA-G molecules

12. A major role for tapasin as a stabilizer of the TAP peptide transporter and consequences for MHC class I expression.

13. 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.

14. 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.

15. 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.

16. 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.

17. 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.

18. Essential for stable expression of the antigen-processing transmembrane domain of the TAP2 protein.

19. 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.

20. 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.

Human TAP Binding Protein (Tapasin) (TAPBP) interaction partners

1. The results demonstrated that the mRNA expression levels of tapasin were significantly downregulated in patients with chronic hepatitis B (CHB) compared with in healthy controls and patients with acute hepatitis B Furthermore, the apoptotic rate of CD8+ T cells was increased in patients with CHB compared with in the other two groups.

2. The disruption of TAP1 and TAPBP generates pluripotent embryonic stem cells with reduced immunogenicity.

3. Fluctuation and entropy analyses show how tapasin chaperones major histocompatibility complex class I by stabilising it in a peptide-receptive conformation.

4. reduction in tapasin expression is associated with tumor progression in colorectal cancer

5. Data suggest that tapasin (Tsn) binds to MHC I with suboptimal cargo and thereby adjusts the energy landscape in favor of MHC I complexes with immunodominant epitopes.

6. TAP/TPN complex formation is driven by hydrophobic interactions via leucine zipper-like motifs.

7. TAP2, HLA-DOA, HLA-DOB, and tapasin loci are novel candidate regions for susceptibility to HCV infection and viral clearance in the Chinese population

8. Analysis of expression of tapasin and/or HLA-I may be of value as prognostic tool for glioblastoma multiforme patients, especially when considering immunotherapy.

9. Modified TAPBP gene function may contribute to the development of refractory chronic rhinosinusitis via reduction of circulating CD8 lymphocytes.

10. Targeted re-sequencing identified rs3106189 at the 5' UTR of TAPBP and rs1052918 at the 3' UTR of TCF3 to be associated with the overall survival of colorectal cancer patients.

11. the data indicate that TAPBPR and tapasin bind in a similar orientation to the same face of MHC class I.

12. TAPBP polymorphisms may play a role in the development of aspirin-exacerbated respiratory disease.

13. isoform lacking exon 3 affects MHC class I-peptide binding

14. Data indicate that the peptide-loading complex (PLC) consists maximally of 2x tapasin-ERp57/MHC I per TAP complex, but one tapasin-ERp57/MHC I in the PLC is essential and sufficient for antigen processing.

15. Tapasin discriminates peptide-human leukocyte antigen-A*02:01 complexes formed with natural ligands.

16. On infection with human cytomegalovirus tapasin mRNA levels were continuously downregulated during infection, while tapasin transcripts remained stable and long-lived.

17. Downregulation of tapasin is associated with a poor clinical outcome for oral squamous cell carcinoma patients and may serve as a prognostic biomarker

18. The interactions of tapasin with both TAP and ERp57 are correlated with strong MHC class I recruitment and assembly enhancement.

19. find that in a competitive situation between high- and low-affinity peptides, tapasin mediates the binding of the high-affinity peptide to class I by accelerating the dissociation of the peptide from an unstable intermediate of the binding reaction.

20. recruits MHC class I molecules to TAP complex during antigen processing