Article
An oncogenic mutation uncouples the v-Jun oncoprotein from positive regulation by the SAPK/JNK pathway in vivo.
Current biology : CB - 15 Jan 1998
May G H, Funk M, Black E J, Clark W, Hussain S, Woodgett J R, Gillespie D A
Abstract excerpt
Stimulation of c-Jun transcriptional activity via phosphorylation mediated by the stress-activated or c-Jun amino-terminal (SAPK/JNK) subgroup of mitogen-activated protein kinases (MAP kinases) is thought to depend on a kinase-docking site (the delta region) within the amino-terminal activation domain, which is deleted from the oncogenic derivative, v-Jun [1] [2] [3]. This mutation markedly enhances v-Jun...
Topics
- Animals
- Gene Expression Regulation
- Humans
- Mitogen-Activated Protein Kinase 12
- Mitogen-Activated Protein Kinases
- Mutation
- Oncogene Protein p65(gag-jun)
- Oncogenes
- Protein Kinases
- Rats
- Recombinant Fusion Proteins
- Signal Transduction