Speculations on the functions of the major heat shock and glucose-regulated proteins

  title={Speculations on the functions of the major heat shock and glucose-regulated proteins},
  author={Hugh R. Pelham},
  • H. Pelham
  • Published 26 September 1986
  • Medicine, Biology
  • Cell

Autoregulation of the Heat-Shock Response

The heat-shock proteins (hsps) were initially defined as a small set of proteins that are rapidly and dramatically induced when cells or whole organisms are exposed to high temperatures1–5 (see Fig.

Heat Shock Proteins and the Regulation of Heat Shock Gene Expression in Eukaryotes

The first chapter is devoted to the general description of stress proteins and peculiarities of their expression in eukaryotic cells and to the modern views of the problem of “negative regulation” of heat shock gene transcription.

The Heat Shock Response: Events Before, During, and After Gene Activation

The use of hyperthermia as a method of treating cancer and another large group of individuals looks at heat shock as a convenient way to activate those genes involved in the synthesis of easily identified proteins.

The heat shock response in human phagocytes.

Heat-shock proteins and development.

Role of heat shock proteins in the formation of stress resistance in different animal strains

In response to heat shock five isoforms of hsp 70 are accumulated in the myocardium of Wistar rats highly resistant to stress in comparison with only 3 isoforms of hsp 70 in August rats with a lower

A role for glyceraldehyde-3-phosphate dehydrogenase in the development of thermotolerance in Xenopus laevis embryos

It is shown that heat shock stimulates increases in the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase and GAPDH, which provides a compelling explanation for the restriction of hsp35 synthesis to the vegetal hemisphere cells of heat-shocked early gastrulae reported previously.

What Are the Mechanisms of Heat Shock Protein-Mediated Cytoprotection Under ATP Deprivation?

This chapter presents some speculations and hypotheses which might, at least in part, clarify how excess HSP(s) compensates for ATP deficiency and maintains the viability of ATP-deprived cells.