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Heat shock (HS) response is a universal mechanism of protection against adverse environmental conditions. It is manifested mainly by rapid and robust induction of molecular chaperones and other cytoprotective proteins. In higher eukaryotes the activation of the HS response is mediated by a master regulator, heat shock transcription factor 1 (HSF1). Here we outline recent progress in understanding the early steps in HSF1 activation by heat in the context of existing models of HSF1 regulation. [ABSTRACT FROM AUTHOR]

It has previously been documented that Zn[sup 2+] inhibits TrkAmediated effects of NGF. To evaluate the ability of Zn[sup 2+] to attenuate the biological activities of NGF mediated by p75[sup NTR], we characterized the effects of this transition metal cation on both binding and the pro-apoptotic properties of the NGFp75[sup NTR] interaction. Binding of NGF to p75[sup NTR] displayed higher affinity in embryonic chick retinal cells than in PC12 cells. NGF induced apoptosis in dissociated cultures of chick neural retina. The addition of 100 µM Zn[sup 2+] inhibited binding and chemical cross-linking of [sup 125]I-NGF to p75[sup NTR], and also attenuated apoptosis mediated by this ligand-receptor interaction. These studies lead to the conclusion that Zn[sup 2+] antagonizes NGF/p75[sup NTR]-mediated signaling, suggesting that the effect of this transition metal cation can be either pro- or anti-apoptotic depending on the cellular context. [ABSTRACT FROM AUTHOR]