MOLECULAR NEUROSCIENCEAnalysis of splicing of four mouse JNK/SAPKα variantsCasanova, Emilio1; Callejo, Ainhoa I.1; Calvo, Pedro1; Chinchetru, Miguel A.1,2Author Information 1Departamento de Bioquímica y Biología Molecular, Universidad de León, 24007 León, Spain 2Corresponding Author: Miguel A. Chinchetru Received 28 September 1999; accepted 14 November 1999 Acknowledgements: This work was supported by a grant from the Junta de Castilla y León (LE36/96). E.C. and A.C. hold a Spanish Ministry of Education Fellowships. We thank V. Revilla for helping with brain sections, and R. Harvey and M. Darlison (Hamburg University) for training with in situ hybridization assays. NeuroReport: February 7, 2000 - Volume 11 - Issue 2 - p 305-309 Buy Abstract The JNK/SAPK (c-Jun NH2-terminal kinase/stress-activated protein kinase) cascade is activated by a variety of stress stimuli and by the inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor α (TNFα). Four splice variants of the mouse JNK/SAPKα isoform, which differ in a region located in subdomains IX–X of the protein, were previously identified. Analysis of the sequence of the central region of the mouse JNK/SAPKα gene indicates that splice variants I and II are generated by a typical alternative splicing mechanism, while splice variants III and IV are generated by a less common mechanism, where alternative 3' splice sites located inside an exon (cryptic sites) are selected. The major splice variants αI and αII have a wide and similar distribution in hippocampus, cerebral cortex, caudate-putamen, amygdala and the granule cell layer of cerebellum, although their expression is specifically regulated in certain cell types. © 2000 Lippincott Williams & Wilkins, Inc.