ArticleThe Journal of biological chemistry2013
Glycan-dependent and -independent interactions contribute to cellular substrate recruitment by calreticulin.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- A chemical-genetic system for calreticulin exposure on cancer cells reveals immune-dependent antitumor effects.Cell death and differentiation · 2026Article
- A genome-wide CRISPR/Cas9 screen identifies calreticulin as a selective repressor of ATF6α.eLife · 2024Article
- Calreticulin P-domain-derived "Eat-me" peptides for enhancing liposomal uptake in dendritic cells.International journal of pharmaceutics · 2024Article
- Optical biosensor based on weak measurement for ultra-sensitive detection of calreticulin in human serum.Biomedical optics express · 2024Article
- Z-αScience advances · 2022Article
- Hematoxylin binds to mutant calreticulin and disrupts its abnormal interaction with thrombopoietin receptor.Blood · 2021Article
- Roles of Calreticulin in Protein Folding, Immunity, Calcium Signaling and Cell Transformation.Progress in molecular and subcellular biology · 2021Article
- Progress in elucidation of molecular pathophysiology of myeloproliferative neoplasms and its application to therapeutic decisions.International journal of hematology · 2020Review
- Neuropathy target esterase (NTE/PNPLA6) and organophosphorus compound-induced delayed neurotoxicity (OPIDN).Advances in neurotoxicology · 2020Article
- Dissecting physical structure of calreticulin, an intrinsically disordered CaJournal of biomolecular structure & dynamics · 2018Article
- Article
- Contributions of the Lectin and Polypeptide Binding Sites of Calreticulin to Its Chaperone Functions in Vitro and in Cells.The Journal of biological chemistry · 2016Article
- The C-Terminal Acidic Region of Calreticulin Mediates Phosphatidylserine Binding and Apoptotic Cell Phagocytosis.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- N-Glycan-based ER Molecular Chaperone and Protein Quality Control System: The Calnexin Binding Cycle.Traffic (Copenhagen, Denmark) · 2016Review
- Oncogenic Drivers in Myeloproliferative Neoplasms: From JAK2 to Calreticulin Mutations.Current hematologic malignancy reports · 2015Review
- Regulation of calreticulin-major histocompatibility complex (MHC) class I interactions by ATP.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- The Aggregatibacter actinomycetemcomitans Cytolethal Distending Toxin Active Subunit CdtB Contains a Cholesterol Recognition Sequence Required for Toxin Binding and Subunit Internalization.Infection and immunity · 2015Article
- N-linked sugar-regulated protein folding and quality control in the ER.Seminars in cell & developmental biology · 2015Review
- The intrinsic and extrinsic effects of N-linked glycans on glycoproteostasis.Nature chemical biology · 2014Review
- Glycoprotein folding and quality-control mechanisms in protein-folding diseases.Disease models & mechanisms · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Calreticulin is an endoplasmic reticulum chaperone with specificity for monoglucosylated glycoproteins. Calreticulin also inhibits precipitation of nonglycosylated proteins and thus contains generic protein-binding sites, but their location and contributions to substrate folding are unknown. We show that calreticulin binds glycosylated and nonglycosylated proteins with similar affinities but distinct interaction kinetics. Although both interactions involve the glycan-binding site or its vicinity, the arm-like proline-rich (P-) domain of calreticulin contributes to binding non/deglycosylated proteins. Correspondingly, ensemble FRET spectroscopy measurements indicate that glycosylated and nonglycosylated proteins induce "open" and "closed" P-domain conformations, respectively. The co-chaperone ERp57 influences substrate-binding kinetics and induces a closed P-domain conformation. Together with analysis of the interactions of calreticulin with cellular proteins, these findings indicate that the recruitment of monoglucosylated proteins to calreticulin is kinetically driven, whereas the P-domain and co-chaperone contribute to stable substrate binding. Substrate sequestration in the cleft between the glycan-binding site and P-domain is a likely mechanism for calreticulin-assisted protein folding.
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Registered trials
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.