The article by Roger J. Davis provides an in-depth review of the JNK group of mitogen-activated protein kinases (MAPKs) and their signaling pathways. JNKs play a crucial role in cellular responses to various environmental and physical cues, including nutrients, growth factors, cytokines, and stress conditions. They are activated through a kinase signaling cascade involving MAPKKs and MAPKKKs. In mammals, three major groups of MAPKs are identified, with JNK being a key component of the stress-activated MAPK pathway. JNK is activated by dual phosphorylation on Thr and Tyr residues, mediated by MAPKKs such as MKK4 and MKK7. These kinases are activated by upstream MAPKKKs, which include MEKKs, MLKs, ASKs, TAK1, and TPL2. The activation of JNK can be regulated by Rho family GTPases and adaptor proteins like TRAFs. JNK signaling is organized by scaffold proteins, such as the JNK interacting protein (JIP) family, which help in the assembly and regulation of the signaling module. The article highlights the role of JNK in stress-induced apoptosis, where it is required for the release of cytochrome c from mitochondria and the activation of caspase-9. However, JNK is not essential for death receptor signaling mediated by caspase-8. The mechanism of JNK's action in apoptotic signaling is still under investigation, but it is suggested that JNK may regulate the stability or function of proteins like p53 and c-Myc. Additionally, the article discusses the role of JNK in cell survival signaling, where transient activation of JNK can be interpreted as a survival signal. JNK also plays a significant role in tumor development, as it is involved in Ras-induced transformation and tumorigenicity. Overall, the review emphasizes the multifaceted roles of JNK in cellular responses and its importance in various physiological and pathological processes.The article by Roger J. Davis provides an in-depth review of the JNK group of mitogen-activated protein kinases (MAPKs) and their signaling pathways. JNKs play a crucial role in cellular responses to various environmental and physical cues, including nutrients, growth factors, cytokines, and stress conditions. They are activated through a kinase signaling cascade involving MAPKKs and MAPKKKs. In mammals, three major groups of MAPKs are identified, with JNK being a key component of the stress-activated MAPK pathway. JNK is activated by dual phosphorylation on Thr and Tyr residues, mediated by MAPKKs such as MKK4 and MKK7. These kinases are activated by upstream MAPKKKs, which include MEKKs, MLKs, ASKs, TAK1, and TPL2. The activation of JNK can be regulated by Rho family GTPases and adaptor proteins like TRAFs. JNK signaling is organized by scaffold proteins, such as the JNK interacting protein (JIP) family, which help in the assembly and regulation of the signaling module. The article highlights the role of JNK in stress-induced apoptosis, where it is required for the release of cytochrome c from mitochondria and the activation of caspase-9. However, JNK is not essential for death receptor signaling mediated by caspase-8. The mechanism of JNK's action in apoptotic signaling is still under investigation, but it is suggested that JNK may regulate the stability or function of proteins like p53 and c-Myc. Additionally, the article discusses the role of JNK in cell survival signaling, where transient activation of JNK can be interpreted as a survival signal. JNK also plays a significant role in tumor development, as it is involved in Ras-induced transformation and tumorigenicity. Overall, the review emphasizes the multifaceted roles of JNK in cellular responses and its importance in various physiological and pathological processes.