1Van Putten V,Refaat Z,Dessev C,et al.Induction of cytosolic phospholipase A2 by oncogenic Ras is mediated through the JNK and ERK pathways in rat epithelial cells[J].The Journal of biological chemistry,2001,276(2):1226-1232.
2Bost F,McKay R,Dean N,et al.The JUN kinase/stress-activated protein kinase pathway is required for epidermal growth factor stimulation of growth of human A549 lung carcinoma cells[J].The Journal of biological chemistry,1997,272(52):33422-33429.
3Xiao L,Lang W.A dominant role for the c-Jun NH2-terminal kinase in oncogenic ras-induced morphologic transformation of human lung carcinoma cells[J].Cancer research,2000,60(2):400-408.
6Katiyar S, Jiao X, Wagner E, et al. Somatic excision demonstrates that c-Jun induces cellular migration and invasion through induction of stem cell factor. Mol Cell Biol, 2007,27:1356-1369.
7Matthews CP,Birkholz AM,Baker AR,et al. Dominant-negative activator protein 1 (TAM67) targets cyclooxygenase-2 and osteopontin under conditions in which it specifically inhibits tumorigenesis. Cancer Res, 2007,67: 2430-2438.
8Sanyal S, Sandstrom D J, Hoeffer CA, et al. AP- 1 function upstream of CREB to control synaptic plasticity in Drosophila. Nature, 2002,416 : 870-874.
9Grondin B,Lefrancois M,Tremblay M, et al. c-Jun homodimers can function as a context-specific coactivator. Mol Cell Biol, 2007,27 : 2919-2933.
10Johnson GL, Nakamura K. The c-Jun kinase/stress-activated pathway: regulation, function and role in human disease. Biochim Biophys Acta,2007, 1773: 1341-1348.
