In this strain, codon 108 in exon 6 of the endogenous mitogen-activated protein kinase 9 (Mapk9 or c-Jun N-terminal kinase 2 (Jnk2)) gene was mutated from a Methionine (ATG) to a Glycine (GGG). Homozygous mice are viable, fertile, and normal in size. Jnk2 exhibits widespread expression and is involved in the regulation of cellular proliferation, transformation, and apoptosis, and has been implicated in some neurodegenerative diseases, diabetes, and arthritis. Phosphorylation of JNK2 by other MAPK kinases is required for activation. This mutation in JNK2MG/MG mice expands the size of the ATP pocket of JNK2, increasing sensitivity to inactive small molecule inhibition by PP1, allowing for specific reversible JNK2 inhibition. These mice exhibit a loss of JNK2 signaling while maintaining expression, and show an increase in cellular proliferation, motility, and survival. These mice may be useful for studying MAP kinase signaling pathways, JNK activation and regulation, and cellular growth.

In this strain, codon 108 in exon 6 of the endogenous mitogen-activated protein kinase 9 (Mapk9 or c-Jun N-terminal kinase 2 (Jnk2)) gene was mutated from a Methionine (ATG) to a Glycine (GGG). These mice may be useful for studying MAP kinase signaling pathways, JNK activation and regulation, and cellular growth.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

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