| Mitogen-activated protein kinase 8/9/10, JNK-46, Stress-activated protein kinase 1c, Stress-activated protein kinase JNK1, c-Jun N-terminal kinase 1, JNK-55, Stress-activated protein kinase 1a, Stress-activated protein kinase JNK2, c-Jun N-terminal kinase 2, MAP kinase p49 3F12, Stress-activated protein kinase 1b, Stress-activated protein kinase JNK3, c-Jun N-terminal kinase 3, MAP kinase 8/9/10, MAPK 8/9/10, SAPK1c, SAPK1a, SAPK1b, MAPK8/9/10, JNK1, PRKM8, SAPK1, SAPK1C, JNK2, PRKM9, SAPK1A, JNK3, JNK3A, PRKM10, SAPK1B |
| JNKs (c-Jun N-terminal kinases) belong to a family of MAP kinases that are involved in a variety of cellular processes, including transcriptional regulation and cellular proliferation, differentiation and development. JNK2 (c-Jun N-terminal kinase 2) and JNK3 (c-Jun N-terminal kinase 3) are 424 and 464 amino acid proteins, respectively, that each contain one protein kinase domain and use magnesium as a cofactor to catalyze the phosphorylation of target proteins, thereby playing a role in a variety of events throughout the cell. Both JNK2 and JNK3 exist as multiple alternatively spliced isoforms and are subject to post-translational phosphorylation on Thr 183 and Thr 221, respectively, an event which activates JNK2/JNK3 enzymatic activity. Defects in the gene encoding JNK3 are a cause of epileptic encephalopathy of the Lennox-Gastaut type, a group of epileptic disorders characterized by severe psychomotor delay and seizures. |
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