ArticleThe international journal of biochemistry & cell biology2010
Activation of heat shock factor 1 plays a role in pyrrolidine dithiocarbamate-mediated expression of the co-chaperone BAG3.
Article in The international journal of biochemistry & cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
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- The Hsp70-Hsp90 go-between Hop/Stip1/Sti1 is a proteostatic switch and may be a drug target in cancer and neurodegeneration.Cellular and molecular life sciences : CMLS · 2021Review
- BAG3 expression and sarcomere localization in the human heart are linked to HSF-1 and are differentially affected by sex and disease.American journal of physiology. Heart and circulatory physiology · 2021Article
- MicroRNAs miR-4535 and miR-1915-5p in amniotic fluid as predictive biomarkers for chorioamnionitis.Future science OA · 2021Article
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- HSF1Base: A Comprehensive Database of HSF1 (Heat Shock Factor 1) Target Genes.International journal of molecular sciences · 2019Article
- Increased expression of heat shock factor 1 (HSF1) is associated with poor survival in gastric cancer patients.Diagnostic pathology · 2018Article
- Roles of heat shock factor 1 beyond the heat shock response.Cellular and molecular life sciences : CMLS · 2018Review
- Effect of BIS depletion on HSF1-dependent transcriptional activation in A549 non-small cell lung cancer cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Article
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- HSP90 inhibitors in the context of heat shock and the unfolded protein response: effects on a primary canine pulmonary adenocarcinoma cell line.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2017Article
- The Role of the Multifunctional BAG3 Protein in Cellular Protein Quality Control and in Disease.Frontiers in molecular neuroscience · 2017Review
- Cardiomyocyte-Specific Human Bcl2-Associated Anthanogene 3 P209L Expression Induces Mitochondrial Fragmentation, Bcl2-Associated Anthanogene 3 Haploinsufficiency, and Activates p38 Signaling.The American journal of pathology · 2016Article
- Development-dependent regulation of molecular chaperones after hypoxia-ischemia.Neurobiology of disease · 2015Article
- Bis is Induced by Oxidative Stress via Activation of HSF1.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014Article
- Chaperone-assisted proteostasis is essential for mechanotransduction in mammalian cells.Communicative & integrative biology · 2013Article
- The Aryl-Hydrocarbon Receptor Protein Interaction Network (AHR-PIN) as Identified by Tandem Affinity Purification (TAP) and Mass Spectrometry.Journal of toxicology · 2013Article
- A chemical cross-linking method for the analysis of binding partners of heat shock protein-90 in intact cells.BioTechniques · 2012Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Adaptive responses to physical and inflammatory stressors are mediated by transcription factors and molecular chaperones. The transcription factor heat shock factor 1 (HSF1) has been implicated in extending lifespan in part by increasing expression of heat shock response genes. Pyrrolidine dithiocarbamate (PDTC) is a small thiol compound that exerts in vivo and in vitro anti-inflammatory properties through mechanisms that remain unclear. Here we report that PDTC induced the release of monomeric HSF1 from the molecular chaperone heat shock protein 90 (Hsp90), with concomitant increase in HSF1 trimer formation, translocation to the nucleus, and binding to promoter of target genes in human HepG2 cells. siRNA-mediated silencing of HSF1 blocked BAG3 gene expression by PDTC. The protein levels of the co-chaperone BAG3 and its interaction partner Hsp72 were stimulated by PDTC in a dose-dependent fashion, peaking at 6h. Inhibition of Hsp90 function by geldanamycin derivatives and novobiocin elicited a pattern of HSF1 activation and BAG3 expression that was similar to PDTC. Chromatin immunoprecipitation studies showed that PDTC and the inhibitor 17-dimethylaminoethylamino-17-demethoxygeldanamycin enhanced the binding of HSF1 to the promoter of several target genes, including BAG3, HSPA1A, HSPA1B, FKBP4, STIP1 and UBB. Cell treatment with PDTC increased significantly the level of Hsp90α thiol oxidation, a posttranslational modification known to inhibit its chaperone function. These results unravel a previously unrecognized mechanism by which PDTC and related compounds could confer cellular protection against inflammation through HSF1-induced expression of heat shock response genes.
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