ArticleThe Journal of biological chemistry2010
Modes of calreticulin recruitment to the major histocompatibility complex class I assembly pathway.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 76 citations in OpenAlex.
- Resistance to the proapoptotic effects of interferon-gamma on melanoma cells used in patient-specific dendritic cell immunotherapy is associated with improved overall survival.Cancer immunology, immunotherapy : CII · 2011Trial
- Reconstitution of glycan-driven MHC-I recycling reveals calreticulin as mediator between TAPBPR and tapasin.The EMBO journal · 2026Article
- Peptide Loading Complex in Cancer: From Peptide Translocation, Editing, and Loading into MHC-I to a Potential Therapeutic Target.Current medical science · 2026Review
- Calcium-mediated calreticulin-IRE1α interaction drives dynamic fluctuation of IRE1α activity under chronic endoplasmic reticulum stress.Nature communications · 2026Article
- Molecular and Functional Analysis of Calcium Binding by a Cancer-linked Calreticulin Mutant.bioRxiv : the preprint server for biology · 2025Article
- Effects of Calreticulin Mutations on HLA Class I Expression in Myeloproliferative Neoplasms.bioRxiv : the preprint server for biology · 2025Article
- Calreticulin-From the Endoplasmic Reticulum to the Plasma Membrane-Adventures of a Wandering Protein.Cancers · 2025Review
- A genome-wide CRISPR/Cas9 screen identifies calreticulin as a selective repressor of ATF6α.eLife · 2024Article
- Introducing Molecular Chaperones into the Causality and Prospective Management of Autoimmune Hepatitis.Digestive diseases and sciences · 2023Review
- Spectroscopic studies of 7,8-diacetoxy-4-methylcoumarin and 7,8-dipentynoyl-4-methylcoumarin binding with calreticulin.Luminescence : the journal of biological and chemical luminescence · 2022Article
- The role of cellular proteostasis in antitumor immunity.The Journal of biological chemistry · 2022Review
- Mechanism of mutant calreticulin-mediated activation of the thrombopoietin receptor in cancers.The Journal of cell biology · 2021Article
- Calreticulin and cancer.Cell research · 2021Review
- Roles of Calreticulin in Protein Folding, Immunity, Calcium Signaling and Cell Transformation.Progress in molecular and subcellular biology · 2021Article
- Calreticulin enhances the secretory trafficking of a misfolded α-1-antitrypsin.The Journal of biological chemistry · 2020Article
- Variations in MHC class I antigen presentation and immunopeptidome selection pathways.F1000Research · 2020Review
- Preferential interaction of MHC class I with TAPBPR in the absence of glycosylation.Molecular immunology · 2019Article
- The Biophysical Interaction of the Danger-Associated Molecular Pattern (DAMP) Calreticulin with the Pattern-Associated Molecular Pattern (PAMP) Lipopolysaccharide.International journal of molecular sciences · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Major histocompatibility complex (MHC) class I molecules are ligands for T-cell receptors of CD8(+) T cells and inhibitory receptors of natural killer cells. Assembly of the heavy chain, light chain, and peptide components of MHC class I molecules occurs in the endoplasmic reticulum (ER). Specific assembly factors and generic ER chaperones, collectively called the MHC class I peptide loading complex (PLC), are required for MHC class I assembly. Calreticulin has an important role within the PLC and induces MHC class I cell surface expression, but the interactions and mechanisms involved are incompletely understood. We show that interactions with the thiol oxidoreductase ERp57 and substrate glycans are important for the recruitment of calreticulin into the PLC and for its functional activities in MHC class I assembly. The glycan and ERp57 binding sites of calreticulin contribute directly or indirectly to complexes between calreticulin and the MHC class I assembly factor tapasin and are important for maintaining steady-state levels of both tapasin and MHC class I heavy chains. A number of destabilizing conditions and mutations induce generic polypeptide binding sites on calreticulin and contribute to calreticulin-mediated suppression of misfolded protein aggregation in vitro. We show that generic polypeptide binding sites per se are insufficient for stable recruitment of calreticulin to PLC substrates in cells. However, such binding sites could contribute to substrate stabilization in a step that follows the glycan and ERp57-dependent recruitment of calreticulin to the PLC.
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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.