Overview:

JNK2 and JNK3 are members of the c-Jun N-terminal kinases (JNKs) which are part of the mitogen-activated protein (MAP) kinase family, and regulate signal transduction in response to environmental stress. JNK2 binds to the c-Jun transactivation domain and phosphorylates it on Ser-63 and Ser-73 (1). JNK2 has been shown to play an important role in disease processes. JNK2 plays a role in ventricular hypertrophy and is thought to be involved in hypertensive cardiac disease (2). JNK3 phosphorylates various transcription factors such as ATF2, Elk-1 and members of the Jun family (3). Activation and nuclear localization of JNK3, a neuronal-specific isoform of JNK, has been associated with hypoxic and ischemic damage of CA1 neurons in the hippocampus. Knockout mice lacking JNK3 showed reduced apoptosis of hippocampal neurons and reduced seizure induced by kainic acid, a glutamate-receptor agonist (4).

References:

1. Sluss, H K. et al: Signal transduction by tumor necrosis factor mediated by JNK protein kinases. Mol Cell Biol. 1994 Dec;14(12):8376-84.

2. Vogel, V. et al: Cardiac hypertrophy in the Prague-hypertensive rat is associated with enhanced JNK2 but not ERK tissue activity. Kidney Blood Press Res. 2001;24(1):52-6.

3. Gupta, S. et al: Selective interaction of JNK protein kinase isoforms with transcription factors. EMBO J. 1996 Jun 3;15(11):2760-70.

4. Yang, D D. et al: Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene. Nature. 1997 Oct 23;389(6653):865-70.