JNK (c-Jun N-Terminal Kinase) MAPK Signaling

Factors causing the activation of JNK1/2 MAPK, includin: osmotic stress, UV irradiation, cytokine withdrawal, mitogenic signaling, and MTA treatment.

There are three genes that encode the JNK MAPK proteins. JNK1 protein is encoded by MAPK8, JNK2 is encoded by MAPK9 and JNK3 is encoded by MAPK10. These genes are alternatively spliced and initiate upwards of 10 different isoforms [Gupta et al.,1996].

JNK1/2 MAPKs activation occurs through mixed-lineage kinases. Upstream MAPKKs such as MAPKK4 and MAPKK7 are phosphorylated and activated by these kinases. In turn, JNK1/2MAPKs are phosphorylated and activated by these upstream MAPKKs.

MAPKKKs such as transforming growth factor β (TGF β)– activated kinase 1 (TAK1) and apoptosis-inducing kinase 1 (ASK1) can also precipitate the activation of JNK1/2 MAPK [Gallo and Johnson, 2002].

Each isoform of JNK MAPK can phosphorylate c-Jun, JunB and JunD. They can also phosphorylate ATF 2, a part of the AP-1 (activator protein-1) transcription factor complex [Davis, 2000]. A range of genes involved in cell cycle progression, cell survival, and apoptosis are targeted by this complex [Wagner and Nebreda, 2009].

The Origin of JNK

JNK was first identified as a participant in apoptosis after growth factors were withdrawn from PC12 pheochromocytoma cells [Xia et al., 1995]. JNK activation and upregulation of the death receptor ligand FaL are the result of over-expression of MEKK1 – an upstream JNK MAPK activator [Faris et al., 1998].

In mice, gene distruption studies have demonstrated the contribution that JNK makes to cell death initiation. In vivo, while JNK1 and JNK2 are necessary for thymocyte apoptosis following the T-cell receptor’s engagement, JNK3 is needed following excitotoxic stress for cell death in hippocampal neurons [Sabapathy et al., 1999; Yang et al., 1997]. Cytochrome C release and apoptosis through the intrinsic cell path can only be stimulated by activating JNK1/2 MAPK. Yet, for JNK1/2 MAPK mediated apoptosis, Bax and Bak are essential [Lei and Davis, 2003].


  • Gupta, S., T. Barrett, et al. (1996). "Selective interaction of JNK protein kinase isoforms with transcription factors." Embo J 15(11): 2760-70.
  • Davis, R. J. (2000). "Signal transduction by the JNK group of MAP kinases." Cell 103(2): 239-52.
  • Gallo, K. A. and G. L. Johnson (2002). "Mixed-lineage kinase control of JNK and p38 MAPK pathways." Nat Rev Mol Cell Biol 3(9): 663-72.
  • Wagner, E. F. and A. R. Nebreda (2009). "Signal integration by JNK and p38 MAPK pathways in cancer development." Nat Rev Cancer 9(8): 537-49.
  • Xia, Z., M. Dickens, et al. (1995). "Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis." Science 270(5240): 1326-31.
  • Faris, M., N. Kokot, et al. (1998). "The c-Jun N-terminal kinase cascade plays a role in stress-induced apoptosis in Jurkat cells by up-regulating Fas ligand expression." J Immunol 160(1): 134-44.
  • Sabapathy, K., Y. Hu, et al. (1999). "JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development." Curr Biol 9(3): 116-25.
  • Yang, D. D., C. Y. Kuan, et al. (1997). "Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene." Nature 389(6653): 865-70.
  • Lei, K. and R. J. Davis (2003). "JNK phosphorylation of Bim-related members of the Bcl2 family induces Bax-dependent apoptosis." Proc Natl Acad Sci USA 100(5): 2432-7.

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Last updated: Apr 1, 2019 at 6:45 AM


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