Titlebook: Stress Proteins; David S. Latchman (Head, Director) Book 1999 Springer-Verlag Berlin Heidelberg 1999 Chaperone.Eiwei?.Gehirn.Heat shock pr

MODE

Regulation of Heat Shock Genes by Cytokines,otic and eukaryotic species have at least 50% identity at the genomic level (Lindquist 1988). It was originally reported that when the chromosomes of the giant salivary gland of . were exposed to elevated temperature, this resulted in areas of swelling on the chromosome known as puffs (Ritossa 1962)

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觀察

Regulation of Heat Shock Transcription Factors by Hypoxia or Ischemia/Reperfusion in the Heart and n developed countries, including myocardial infarction, cerebral ischemia and embolic vascular occlusions of other tissues. Recent advances in diagnosis and treatment have allowed, at an early stage, the rapid return of blood flow by surgical, interventional or pharmacological means, to prevent infa

易受刺激

Autoregulation of the Heat Shock Response,s of heat shock proteins and the biochemical properties of molecular chaperones is essential to prevent nascent polypeptides from premature non-productive interactions and to protect non-native proteins from misfolding and aggregation. Under conditions of normal cell growth, heat shock proteins are

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The Cellular Stress Gene Response in Brain,ms have been made using mammalian cells grown in tissue culture (Morimoto 1993; Morimoto et al. 1994; see also Chap. 3, this volume). Recently, an increasing amount of work has been carried out on intact thermoregulating animals. As will be shown in this article, the heat shock response is physiolog

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Heat Stress Proteins and Their Relationship to Myocardial Protection,ive, awaiting the complications of ischaemic injury, but has entered a new era where the mortality of acute myocardial infarction can be approximately halved by thrombolytic agents and aspirin (ISIS-2 1988), with the greatest benefit seen in those treated soon after the onset of symptoms. The lack o

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Heat Shock Proteins in Inflammation and Immunity,isms and, on the other, is involved in a broad spectrum of diseases. According to the initiating event, the inflammatory response may involve, or not, an antigenspecific immune response. In the first case, the initiating agent is generally a microorganism or an antigen of unknown origin, while in th

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Heat Shock Proteins in Embryonic Development,at shock proteins (Hsps) were described as active partners in cell differentiation and organism morphogenesis. Let us mention two such observations. As early as 1982, the variations in small Hsp expression during . development were described (Sirotkin and Davidson 1982). As we shall see, the express

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Indigence

Heat Shock Protein 60 and Type I Diabetes,y. During the clinically silent, early stages of disease the pancreas is infiltrated by inflammatory cells which mediate beta cell damage. The failure of glucose homeostasis observed in patients is a direct consequence of immunologically mediated beta cell destruction. While there is general agreeme