Analysis of splicing of four mouse JNK/SAPK alpha variants

The JNK/SAPK (c-Jun NH2-terminal kinase/stress-activated protein kinase) ca scade is activated by a variety of stress stimuli and by the inflammatory c ytokines interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF alpha). Four splice variants of the mouse JNK/SAPK alpha isoform, which differ in a region located in subdomains IX-X of the protein, were previously identifi ed. Analysis of the sequence of the central region of the mouse JNK/SAPK al pha gene indicates that splice variants I and II are generated by a typical alternative splicing mechanism, while splice variants III and IV are gener ated by a less common mechanism, where alternative 3' splice sites located inside an exon (cryptic sites) are selected. The major splice variants alph a I and alpha II have a wide and similar distribution in hippocampus, cereb ral cortex, caudate-putamen, amygdala and the granule cell layer of cerebel lum although their expression is specifically regulated in certain cell typ es. NeuroReport 11:305-309 (C) 2000 Lippincott Williams & Wilkins.