ArticleJournal of cell science2012
Limitation of individual folding resources in the ER leads to outcomes distinct from the unfolded protein response.
Article in Journal of cell science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Comparative Meta-Analysis of Transcriptomics Data during Cellular Senescence and In Vivo Tissue Ageing.Oxidative medicine and cellular longevity · 2015Pooled it
- Mitogenome and Phylogeny of the Hairy Puffer Pao baileyi (Sontirat 1985).Biochemical genetics · 2026Article
- CCDC134 controls TLR biogenesis through the ER chaperone Gp96.The Journal of experimental medicine · 2025Article
- Deficient glycan extension and endoplasmic reticulum stresses in ALG3-CDG.Journal of inherited metabolic disease · 2024Article
- Tracing genetic diversity captures the molecular basis of misfolding disease.Nature communications · 2024Article
- Nogo-A Mediated Endoplasmic Reticulum Stress During Myocardial Ischemic-Reperfusion Injury in Diabetic Rats.Cardiovascular toxicology · 2023Article
- Insulin secretion deficits in a Prader-Willi syndrome β-cell model are associated with a concerted downregulation of multiple endoplasmic reticulum chaperones.PLoS genetics · 2023Article
- Glucose-Regulated Protein 94 (GRP94): A Novel Regulator of Insulin-Like Growth Factor Production.Cells · 2020Review
- Protein quality control in the secretory pathway.The Journal of cell biology · 2019Review
- Endoplasmic Reticulum Chaperone Glucose-Regulated Protein 94 Is Essential for Proinsulin Handling.Diabetes · 2019Article
- HSP-4/BiP expression in secretory cells is regulated by a developmental program and not by the unfolded protein response.PLoS biology · 2019Article
- Roles of the endoplasmic reticulum-resident, collagen-specific molecular chaperone Hsp47 in vertebrate cells and human disease.The Journal of biological chemistry · 2019Review
- A Human Variant of Glucose-Regulated Protein 94 That Inefficiently Supports IGF Production.Endocrinology · 2016Article
- Grp94 Protein Delivers γ-Aminobutyric Acid Type A (GABAA) Receptors to Hrd1 Protein-mediated Endoplasmic Reticulum-associated Degradation.The Journal of biological chemistry · 2016Article
- PDIA6 regulates insulin secretion by selectively inhibiting the RIDD activity of IRE1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Recombinant Newcastle disease virus (rL-RVG) triggers autophagy and apoptosis in gastric carcinoma cells by inducing ER stress.American journal of cancer research · 2016Article
- Depletion of the thiol oxidoreductase ERp57 in tumor cells inhibits proliferation and increases sensitivity to ionizing radiation and chemotherapeutics.Oncotarget · 2015Article
- The unfolded protein response in glioblastomas: targetable or trouble?Future science OA · 2015Review
- Unfolding the unfolded protein response: unique insights into brain ischemia.International journal of molecular sciences · 2015Review
- Dynamics of unfolded protein response in recombinant CHO cells.Cytotechnology · 2015Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
ER stress leads to upregulation of multiple folding and quality control components, known as the unfolded protein response (UPR). Glucose Regulated Protein 78 (GRP78) (also known as binding immunoglobulin protein, BiP, and HSPA5) and GRP94 are often upregulated coordinately as part of this homeostatic response. Given that endoplasmic reticulum (ER) chaperones have distinct sets of clients, we asked how cells respond to ablation of individual chaperones. The cellular responses to silencing BiP, GRP94, HSP47, PDIA6 and OS-9, were distinct. When BiP was silenced, a widespread UPR was observed, but when GRP94 was either inhibited or depleted by RNA interference (RNAi), the expression of only some genes was induced, notably those encoding BiP and protein disulfide isomerase A6 (PDIA6). Silencing of HSP47 or OS-9 did not lead to any compensatory induction of other genes. The selective response to GRP94 depletion was distinct from a typical ER stress response, both because other UPR target genes were not affected and because the canonical UPR signaling branches were not activated. The response to silencing of GRP94 did not preclude further UPR induction when chemical stress was imposed. Importantly, re-expression of wild-type GRP94 in the silenced cells prevented the upregulation of BiP and PDIA6, whereas re-expression of an ATPase-deficient GRP94 mutant did not, indicating that cells monitor the activity state of GRP94. These findings suggest that cells are able to distinguish among folding resources and generate distinct responses.
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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.