ArticleThe Journal of biological chemistry2014
Depletion of cyclophilins B and C leads to dysregulation of endoplasmic reticulum redox homeostasis.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
- Biophysical characterization of Cyclophilin B reveals membrane localization as its primary functional determinant as a prolyl isomerase.Protein science : a publication of the Protein Society · 2026Article
- Human Cyclophilins-An Emerging Class of Drug Targets.Medicinal research reviews · 2026Review
- Macrophages signal cross-talks under hyperglycemic conditions and their link to cyclophilins.Molecular medicine (Cambridge, Mass.) · 2026Article
- SRPS: Survival Reinforced Transfer Learning for Multicentric Proteomic Subtyping and Biomarker Discovery.Genomics, proteomics & bioinformatics · 2025Article
- LONP1 regulation of mitochondrial protein folding provides insight into beta cell failure in type 2 diabetes.Nature metabolism · 2025Article
- Cyclophilin A and C are the Main Components of Extracellular Vesicles in Response to Hyperglycemia in BV2 Microglial Cells.Molecular neurobiology · 2025Article
- DR5 Disulfide Bonding Functions as a Sensor and Effector of Protein Folding Stress.Molecular cancer research : MCR · 2025Article
- Integrated Multi-Omics Analysis of Cerebrospinal Fluid in Postoperative Delirium.Biomolecules · 2024Article
- Endoplasmic Reticulum Stress and Its Impact on Adipogenesis: Molecular Mechanisms Implicated.Nutrients · 2023Review
- Article
- Human Cyclophilin B Nuclease Activity Revealed via Nucleic Acid-Based Electrochemical Sensors.Angewandte Chemie (International ed. in English) · 2022Article
- Chaperoning activity of the cyclophilin family prevents tau aggregation.Protein science : a publication of the Protein Society · 2022Article
- Furanoditerpenes fromACS chemical neuroscience · 2022Article
- Increase of serum cyclophilin C levels in the follow-up of coronary artery disease: A biomarker and possible clinical predictor.Archivos de cardiologia de Mexico · 2022Article
- Peptidylprolyl isomerase C (Ppic) regulates invariant Natural Killer T cell (iNKT) differentiation in mice.European journal of immunology · 2021Article
- Cyclophilins A, B, and C Role in Human T Lymphocytes Upon Inflammatory Conditions.Frontiers in immunology · 2021Article
- CaBMC biology · 2020Article
- High Serum Cyclophilin C levels as a risk factor marker for Coronary Artery Disease.Scientific reports · 2019Article
- Pharmacological Targeting of the ER-Resident Chaperones GRP94 or Cyclophilin B Induces Secretion of IL-22 Binding Protein Isoform-1 (IL-22BPi1).International journal of molecular sciences · 2019Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Protein folding within the endoplasmic reticulum is assisted by molecular chaperones and folding catalysts that include members of the protein-disulfide isomerase and peptidyl-prolyl isomerase families. In this report, we examined the contributions of the cyclophilin subset of peptidyl-prolyl isomerases to protein folding and identified cyclophilin C as an endoplasmic reticulum (ER) cyclophilin in addition to cyclophilin B. Using albumin and transferrin as models of cis-proline-containing proteins in human hepatoma cells, we found that combined knockdown of cyclophilins B and C delayed transferrin secretion but surprisingly resulted in more efficient oxidative folding and secretion of albumin. Examination of the oxidation status of ER protein-disulfide isomerase family members revealed a shift to a more oxidized state. This was accompanied by a >5-fold elevation in the ratio of oxidized to total glutathione. This "hyperoxidation" phenotype could be duplicated by incubating cells with the cyclophilin inhibitor cyclosporine A, a treatment that triggered efficient ER depletion of cyclophilins B and C by inducing their secretion to the medium. To identify the pathway responsible for ER hyperoxidation, we individually depleted several enzymes that are known or suspected to deliver oxidizing equivalents to the ER: Ero1αβ, VKOR, PRDX4, or QSOX1. Remarkably, none of these enzymes contributed to the elevated oxidized to total glutathione ratio induced by cyclosporine A treatment. These findings establish cyclophilin C as an ER cyclophilin, demonstrate the novel involvement of cyclophilins B and C in ER redox homeostasis, and suggest the existence of an additional ER oxidative pathway that is modulated by ER cyclophilins.
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Registered trials
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