Abstract:
:Protein synthesis in all cells is readily interrupted by environmental stresses such as hyperthermia. However, stressed cells also have mechanisms which, even under conditions where normal protein synthesis is completely inhibited, allow them to synthesise a group of highly conserved proteins--the so-called heat shock proteins (HSP). Some of these proteins are now known to facilitate the recovery of normal RNA processing and protein synthesis after exposure to hyperthermia and to protect the cell against further damage. They also play an important role in the synthesis and transport of normal proteins in unstressed cells, and perhaps also the export from cells of abnormal proteins of host or viral origin. Synthesis of HSP is also triggered by exposure to stresses other than hyperthermia, for example heavy metals (e.g. gold complexes), thiol-reactive chemicals, near UV radiation, viruses, oxyradicals and certain cytokines. Furthermore, there are also a number of proteins which are induced by these physicochemical stresses but not by heat; for this reason "stress protein" will be used as a general term to describe both HSP and related, physicochemically-induced, proteins. The cysteine-rich metallothioneins, which behave in some respects as stress proteins, will not be included in this review. Because many of the factors which stimulate stress protein induction occur during inflammatory and immune responses, there has been increasing interest in the possible role of stress proteins in inflammatory disease such as arthritis. The purpose of this article is to review the basic biochemical mechanisms involved in the induction of stress proteins and offer some speculations on their potential role in rheumatic disease.
journal_name
Rheumatol Intjournal_title
Rheumatology internationalauthors
Hurst NPdoi
10.1007/BF00541323subject
Has Abstractpub_date
1990-01-01 00:00:00pages
271-6issue
6eissn
0172-8172issn
1437-160Xjournal_volume
9pub_type
杂志文章,评审abstract::The neutrophilic granule protein proteinase 3 (PR3) is the preferred target antigen of anti-neutrophil cytoplasmic antibodies (ANCA) found in the serum of patients with Wegener's granulomatosis, a systemic small-vessel vasculitis. Due to the lack of data concerning the murine homologue of human PR3, we assessed the ne...
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更新日期:2007-08-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章,随机对照试验
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更新日期:2010-11-01 00:00:00
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journal_title:Rheumatology international
pub_type: 杂志文章,多中心研究,随机对照试验
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更新日期:2010-09-01 00:00:00
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journal_title:Rheumatology international
pub_type: 杂志文章
doi:10.1007/s00296-012-2431-3
更新日期:2013-03-01 00:00:00
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journal_title:Rheumatology international
pub_type: 杂志文章
doi:10.1007/s00296-007-0465-8
更新日期:2008-03-01 00:00:00
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pub_type: 杂志文章,多中心研究
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journal_title:Rheumatology international
pub_type: 杂志文章
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更新日期:2005-05-01 00:00:00
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journal_title:Rheumatology international
pub_type: 杂志文章
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更新日期:2008-11-01 00:00:00
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pub_type: 杂志文章
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更新日期:2013-10-01 00:00:00
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更新日期:2016-03-01 00:00:00
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journal_title:Rheumatology international
pub_type: 杂志文章
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更新日期:2010-05-01 00:00:00
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pub_type: 杂志文章
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更新日期:2019-06-01 00:00:00
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journal_title:Rheumatology international
pub_type: 杂志文章
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更新日期:1985-01-01 00:00:00
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journal_title:Rheumatology international
pub_type: 杂志文章
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更新日期:2005-08-01 00:00:00
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pub_type: 杂志文章
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更新日期:2013-07-01 00:00:00