Focal adhesion kinase expressed by nerve cell lines shows increased tyrosine phosphorylation in response to Alzheimer's A beta peptide.

摘要: A beta is a 39-43-amino acid peptide that accumulates as extracellular aggregates in Alzheimer's disease-afflicted brain tissue. Contact between these and neurons potentially pathogenic, although little known about the cellular transduction mechanisms. We have investigated impact of on neuronal control protein tyrosine phosphorylation, which underlies signal for multiple families growth factor adhesion receptors. Added to cultures rat human nerve cell lines, evoked non-desensitizing increase (1.3-3.6-fold) phosphorylation band at 118 kDa. The 118-kDa was determined by immunoprecipitation be pp125FAK, not previously documented cells lineage. Immunoblots with anti-focal kinase (FAK) showed had no effect FAK levels. occurred doses lactate dehydrogenase release; preceded first detectable release 4 h. Like degeneration, response dependent aggregation differentiation. Since essential its activity component integrin-, peptide-, lysophosphatidic acid-mediated signaling, data establish link pathways implicated diverse functions including neurite outgrowth, cycle, apoptosis.