ArticleMolecular biology of the cell2010
Functional relationship between protein disulfide isomerase family members during the oxidative folding of human secretory proteins.
Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
60 citing papers in PubMed, 87 citations in OpenAlex.
- Unfolded Protein Response Pathways in Cancer: Mechanisms, Tumor Biology and Therapeutic Opportunities.Molecular diagnosis & therapy · 2026Review
- Thiol Isomerases: Enzymatic Mechanisms, Models of Oxidation, and Antagonism by Galloylated Polyphenols.Antioxidants (Basel, Switzerland) · 2025Review
- Activity-Based Protein Profiling Identifies Protein Disulfide-Isomerases as Target Proteins of the Volatile Salinilactones.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Protein disulfide isomerase family mediated redox regulation in cancer.Advances in cancer research · 2023Review
- PDIA3/ERp57 promotes a matrix-rich secretome that stimulates fibroblast adhesion through CCN2.American journal of physiology. Cell physiology · 2022Article
- Distinct roles and actions of protein disulfide isomerase family enzymes in catalysis of nascent-chain disulfide bond formation.iScience · 2021Article
- Protein disulphide isomerase inhibition as a potential cancer therapeutic strategy.Cancer medicine · 2021Review
- In oxygen-deprived tumor cells ERp57 provides radioprotection and ensures proliferation via c-Myc, PLK1 and the AKT pathway.Scientific reports · 2021Article
- Tumor cells rely on the thiol oxidoreductase PDI for PERK signaling in order to survive ER stress.Scientific reports · 2020Article
- The Redox Activity of Protein Disulfide Isomerase Inhibits ALS Phenotypes in Cellular and Zebrafish Models.iScience · 2020Article
- Hypoxia evokes increased PDI and PDIA6 expression in the infarcted myocardium of ex-germ-free and conventionally raised mice.Biology open · 2019Article
- Methods to identify the substrates of thiol-disulfide oxidoreductases.Protein science : a publication of the Protein Society · 2019Review
- Lipase maturation factor 1 affects redox homeostasis in the endoplasmic reticulum.The EMBO journal · 2018Article
- Ufm1-Specific Ligase Ufl1 Regulates Endoplasmic Reticulum Homeostasis and Protects Against Heart Failure.Circulation. Heart failure · 2018Article
- Biosynthesis, structure, and folding of the insulin precursor protein.Diabetes, obesity & metabolism · 2018Review
- Redox Regulation of Mitochondrial Fission Protein Drp1 by Protein Disulfide Isomerase Limits Endothelial Senescence.Cell reports · 2018Article
- Production of complex viral glycoproteins in plants as vaccine immunogens.Plant biotechnology journal · 2018Review
- Succination of Protein Disulfide Isomerase Links Mitochondrial Stress and Endoplasmic Reticulum Stress in the Adipocyte During Diabetes.Antioxidants & redox signaling · 2017Article
- 'Something in the way she moves': The functional significance of flexibility in the multiple roles of protein disulfide isomerase (PDI).Biochimica et biophysica acta. Proteins and proteomics · 2017Review
- ER-associated degradation is required for vasopressin prohormone processing and systemic water homeostasis.The Journal of clinical investigation · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
To examine the relationship between protein disulfide isomerase family members within the mammalian endoplasmic reticulum, PDI, ERp57, ERp72, and P5 were depleted with high efficiency in human hepatoma cells, either singly or in combination. The impact was assessed on the oxidative folding of several well-characterized secretory proteins. We show that PDI plays a predominant role in oxidative folding because its depletion delayed disulfide formation in all secretory proteins tested. However, the phenotype was surprisingly modest suggesting that other family members are able to compensate for PDI depletion, albeit with reduced efficacy. ERp57 also exhibited broad specificity, overlapping with that of PDI, but with preference for glycosylated substrates. Depletion of both PDI and ERp57 revealed that some substrates require both enzymes for optimal folding and, furthermore, led to generalized protein misfolding, impaired export from the ER, and degradation. In contrast, depletion of ERp72 or P5, either alone or in combination with PDI or ERp57 had minimal impact, revealing a narrow substrate specificity for ERp72 and no detectable role for P5 in oxidative 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.