Biological Information | |
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Background Information: | c-Jun N-terminal kinases (JNKs), a stress-activated protein kinase (SAPK), is involved in cellular responses to environmental stresses. JNK kinases can be activated by stimuli such as UV light, radiation, protein synthesis inhibitors, ceramide, DNA-damaging drugs, chemopreventive drugs, TNF-a, and interleukin 1. JNK binds to an NH2-terminal region of ATF2 and c-Jun and phosphorylates two sites within the activation domain of each transcription factor. Three JNK genes (Jnk1, -2 and -3) have been identified in humans; however, splice variants result in a total of 10 isoforms. Inhibition of JNK3 (MAPK10, Mitogen-activated protein kinase 10, Stress-activated protein kinase JNK3) may provide clinical benefit in diseases as diverse as immune inflammatory (joint, bowel, pulmonary), ischemic injury (brain, cardiac) and neurodegenerative (Alzheimer's, Parkinson's) diseases. |
Target Class: | Kinase |
Family: | Ser/Thr Kinase; MAPK; JNK subfamily |
Accession Number: | NM_002753.2; NM_138980.1; NM_138981.1; NM_138982.1 |
Target Name: | JNK3/SAPK1b |
Target Aliases: | MAPK10, JNK3A, p54bSAPK, PRKM10, FLJ12099, JNK3, p493F12, MGC50974, FLJ33785 |
Target Species: | Human |
Usage | |
Product Type: | Enzymes |
Application: | Drug Discovery & Development |
Storage Conditions: | 6 months at -70°C |
Usage Disclaimer: | These products may be covered by issued US and/or foreign patents, patent application and subject to Limited Use Label License. Please visit discoverx.com/license for a list of products that are governed by limited use label license terms and relevant patent and trademark information. |
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