ArticlePloS one2010
Identification of gp96 as a novel target for treatment of autoimmune disease in mice.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Trial
- Interplay between the Chaperone System and Gut Microbiota Dysbiosis in Systemic Lupus Erythematosus Pathogenesis: Is Molecular Mimicry the Missing Link between Those Two Factors?International journal of molecular sciences · 2024Review
- Glycoprotein 96 in Peritoneal Dialysis Effluent-Derived Extracellular Vesicles: A Tool for Evaluating Peritoneal Transport Properties and Inflammatory Status.Frontiers in immunology · 2022Article
- The Pathophysiological Role of Heat Shock Response in Autoimmunity: A Literature Review.Cells · 2021Review
- Inhibition of Hsp90 Counteracts the Established Experimental Dermal Fibrosis Induced by Bleomycin.Biomedicines · 2021Article
- Aminoacyl-tRNA synthetases as therapeutic targets.Nature reviews. Drug discovery · 2019Review
- Association of HSP90B1 genetic polymorphisms with efficacy of glucocorticoids and improvement of HRQoL in systemic lupus erythematosus patients from Anhui Province.American journal of clinical and experimental immunology · 2018Article
- Anti-Hsp90 therapy in autoimmune and inflammatory diseases: a review of preclinical studies.Cell stress & chaperones · 2016Review
- Hsp90 blockade modulates bullous pemphigoid IgG-induced IL-8 production by keratinocytes.Cell stress & chaperones · 2014Article
- Detection of novel auto-antigens in patients with recurrent miscarriage: description of an approach and preliminary findings.Croatian medical journal · 2014Article
- Inhibitory effects of heat shock protein 90 blockade on proinflammatory human Th1 and Th17 cell subpopulations.Journal of inflammation (London, England) · 2014Article
- Glucose-regulated proteins in cancer: molecular mechanisms and therapeutic potential.Nature reviews. Cancer · 2014Review
- Cellular stress response and innate immune signaling: integrating pathways in host defense and inflammation.Journal of leukocyte biology · 2013Review
- Essential nontranslational functions of tRNA synthetases.Nature chemical biology · 2013Review
- The role of glycoprotein 96 in the persistent inflammation of rheumatoid arthritis.Archives of biochemistry and biophysics · 2013Review
- Article
- Aberrant expression and secretion of heat shock protein 90 in patients with bullous pemphigoid.PloS one · 2013Article
- Heat shock protein 90 inhibition by 17-DMAG lessens disease in the MRL/lpr mouse model of systemic lupus erythematosus.Cellular & molecular immunology · 2012Article
- Role of hsp90 in systemic lupus erythematosus and its clinical relevance.Autoimmune diseases · 2012Article
- HSP70i is a critical component of the immune response leading to vitiligo.Pigment cell & melanoma research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heat shock proteins have been implicated as endogenous activators for dendritic cells (DCs). Chronic expression of heat shock protein gp96 on cell surfaces induces significant DC activations and systemic lupus erythematosus (SLE)-like phenotypes in mice. However, its potential as a therapeutic target against SLE remains to be evaluated. In this work, we conducted chemical approach to determine whether SLE-like phenotypes can be compromised by controlling surface translocation of gp96. From screening of chemical library, we identified a compound that binds and suppresses surface presentation of gp96 by facilitating its oligomerization and retrograde transport to endoplasmic reticulum. In vivo administration of this compound reduced maturation of DCs, populations of antigen presenting cells, and activated B and T cells. The chemical treatment also alleviated the SLE-associated symptoms such as glomerulonephritis, proteinuria, and accumulation of anti-nuclear and -DNA antibodies in the SLE model mice resulting from chronic surface exposure of gp96. These results suggest that surface translocation of gp96 can be chemically controlled and gp96 as a potential therapeutic target to treat autoimmune disease like SLE.
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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.