ArticleMolecular immunology2019
Preferential interaction of MHC class I with TAPBPR in the absence of glycosylation.
Article in Molecular immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Reconstitution of glycan-driven MHC-I recycling reveals calreticulin as mediator between TAPBPR and tapasin.The EMBO journal · 2026Article
- Identification of novel HLA class I-restricted hepatitis B virus peptides and their modulation by peptide editor TAPBPR.Frontiers in immunology · 2026Article
- TAPBPR promotes editing of the HLA-B44 peptide repertoire, increasing the presentation of peptides containing a C-terminal tryptophan.Frontiers in immunology · 2025Article
- Reanalysis of Immunopeptidomics Datasets Provides Mechanistic Insight into TAPBPR-Mediated Peptide Editing on HLA-A, -B and -C Molecules.Wellcome open research · 2024Article
- Molecular basis of MHC I quality control in the peptide loading complex.Nature communications · 2022Article
- TAPBPR employs a ligand-independent docking mechanism to chaperone MR1 molecules.Nature chemical biology · 2022Article
- Chaperones and Catalysts: How Antigen Presentation Pathways Cope With Biological Necessity.Frontiers in immunology · 2022Review
- The glycosylation status of MHC class I molecules impacts their interactions with TAPBPR.Molecular immunology · 2021Article
- A Highly Complex, MHC-Linked, 350 Million-Year-Old Shark Nonclassical Class I Lineage.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Partnering for the major histocompatibility complex class II and antigenic determinant requires flexibility and chaperons.Current opinion in immunology · 2021Review
- TAPBPR promotes antigen loading on MHC-I molecules using a peptide trap.Nature communications · 2021Article
- Construction and Validation of an Immune Infiltration-Related Gene Signature for the Prediction of Prognosis and Therapeutic Response in Breast Cancer.Frontiers in immunology · 2021Article
- Molecular determinants of chaperone interactions on MHC-I for folding and antigen repertoire selection.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Distinct Polymorphisms in HLA Class I Molecules Govern Their Susceptibility to Peptide Editing by TAPBPR.Cell reports · 2019Article
- Article
- Utilizing TAPBPR to promote exogenous peptide loading onto cell surface MHC I molecules.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We recently discovered that TAPBPR promotes reglucosylation of the N-linked glycan on MHC class I molecules, a modification that restores their recognition by calreticulin and reincorporation into the peptide-loading complex. We wondered whether TAPBPR displayed some degree of glycan specificity, as is known to be the case for tapasin via its interaction with calreticulin & ERp57, or whether its interaction with MHC class I was glycan independent. Here, we explored this by comparing the ability of TAPBPR to bind to MHC class I containing either an intact or disrupted NxS/T glycosylation consensus sequence. In contrast to tapasin, TAPBPR bound strongly to MHC class I molecules that lacked N-linked glycosylation, suggesting that the TAPBPR:MHC class I interaction is glycan independent. Furthermore, we found that glycosylated HLA-A2 preferentially interacts with tapasin rather than TAPBPR, possibly explaining, in part, why MHC class I molecules bind efficiently to tapasin in the face of an alternative chaperone. The distinction in glycan specificity between the two peptide editors suggests that TAPBPR may bind to MHC class I molecules that are associated with a broader diversity of oligosaccharides attached compared with tapasin. This may explain, to some extent, the ability of TAPBPR to interact with MHC class I molecules outside of the ER.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.