Cerebral ischemia is a simple model to give a stress to the nervous system and to change signal transduction, growth regulation, and neuronal differentiation, which should activate some transcription factors and induce heat shock protein 70 (HSP70), or amyloid precursor protein gene expression. An essential part of gene expression and regulation is the binding of a regulatory protein to the recognition sequence of the appropriate gene. A novel protein motif for nucleic acid recognition called “zinc finger” is one such transcription factor. A relationship between gene expressions of a transcription factor and HSP70 has been suggested. Zinc finger gene is normally expressed in rat cerebral cortex, and is induced by transient ischemia with a maximum at 1 h after the 30 min of transient occlusion of middle cerebral artery. In contrast, HSP70 mRNA is not expressed in normal condition, but is greatly induced by transient ischemia with a maximum at 8 h of reperfusion. In an attempt to examine a possible relationship between heat shock stress and an induction of amyloid precursor protein, cultured lymphoblastoid cells established from twelve human subjects were treated with heat shock.
- Kunitztype serine protease inhibitor
- amyloid precursor protein
- heat shock protein
- heatshock cognate protein
ASJC Scopus subject areas