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https://olympias.lib.uoi.gr/jspui/handle/123456789/19335Full metadata record
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Lee, B. S. | en |
| dc.contributor.author | Chen, J. | en |
| dc.contributor.author | Angelidis, C. | en |
| dc.contributor.author | Jurivich, D. A. | en |
| dc.contributor.author | Morimoto, R. I. | en |
| dc.date.accessioned | 2015-11-24T18:59:01Z | - |
| dc.date.available | 2015-11-24T18:59:01Z | - |
| dc.identifier.issn | 0027-8424 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/19335 | - |
| dc.rights | Default Licence | - |
| dc.subject | DNA-Binding Proteins/genetics/*metabolism | en |
| dc.subject | Gene Expression/drug effects | en |
| dc.subject | HeLa Cells | en |
| dc.subject | Heat-Shock Proteins/genetics/*metabolism | en |
| dc.subject | Hot Temperature | en |
| dc.subject | Humans | en |
| dc.subject | Indomethacin/*pharmacology | en |
| dc.subject | Inflammation/drug therapy/genetics/metabolism | en |
| dc.subject | Phosphorylation | en |
| dc.subject | Stress, Physiological/genetics/metabolism | en |
| dc.subject | Transcription Factors | en |
| dc.title | Pharmacological modulation of heat shock factor 1 by antiinflammatory drugs results in protection against stress-induced cellular damage | en |
| heal.type | journalArticle | - |
| heal.type.en | Journal article | en |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/7638169 | - |
| heal.identifier.secondary | http://www.pnas.org/content/92/16/7207.full.pdf | - |
| heal.language | en | - |
| heal.access | campus | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
| heal.publicationDate | 1995 | - |
| heal.abstract | The activation of heat shock genes by diverse forms of environmental and physiological stress has been implicated in a number of human diseases, including ischemic damage, reperfusion injury, infection, neurodegeneration, and inflammation. The enhanced levels of heat shock proteins and molecular chaperones have broad cytoprotective effects against acute lethal exposures to stress. Here, we show that the potent antiinflammatory drug indomethacin activates the DNA-binding activity of human heat shock transcription factor 1 (HSF1). Perhaps relevant to its pharmacological use, indomethacin pretreatment lowers the temperature threshold of HSF1 activation, such that a complete heat shock response can be attained at temperatures that are by themselves insufficient. The synergistic effect of indomethacin and elevated temperature is biologically relevant and results in the protection of cells against exposure to cytotoxic conditions. | en |
| heal.journalName | Proc Natl Acad Sci U S A | en |
| heal.journalType | peer-reviewed | - |
| heal.fullTextAvailability | TRUE | - |
| Appears in Collections: | Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ | |
Files in This Item:
| File | Description | Size | Format | |
|---|---|---|---|---|
| Lee-1995-Pharmacological modu.pdf | 1.65 MB | Adobe PDF | View/Open |
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