The c-Jun N-terminal kinases (JNKs)/stress-activated protein kinases are intracellular protein kinases that play a key central role in the transduction of extracellular signals to potentiate cellular responses. JNKs are tightly regulated and are essential for regulating many physiological processes, including cell proliferation, differentiation, proliferation, death, and survival and inflammation. Thus, JNK disregulation contributes to the development of several different diseases, such as type 2 diabetes, obesity, inflammation, neurodegenerative disorders, and cancer. The present review summarizes the recent findings regarding the distinct roles of the three JNK members: JNK1, JNK2, and JNK3. JNK1 and JNK2 are ubiquitously expressed and have both redundant and opposing functions. The mounting evidence for the role of JNK activation in the development of cancer and other diseases has spurred interest in JNK inhibitors as a therapeutic approach for diseases. A strong understanding of the tissue-specific roles of the three JNK members, in combination with therapeutics that have high on-target specificity, will be the key to the successful therapeutic inhibition of JNK. In this chapter, we summarize the evidence that demonstrates the importance of JNK in the development of cancer and other diseases and review the current advances and challenges in the development of JNK inhibitors.
c-Jun JNK SAPK MAPK SP600125
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