![]() ![]() Next, the activated MAP3Ks transmit the signals to kinases at the MAPKK level, which are mainly MKK4 and MKK7. Those receptors or receptor-independent stress-induced membranal changes further transmit the signals to adaptor proteins that can by themselves activate kinases in the MAP4K, and sometime, MAP3K tiers of the JNK cascade. The JNK module is activated by environmental stresses (ionizing radiation, heat, oxidative stress, and DNA damage) and inflammatory cytokines, as well as growth factors, and signaling to the JNK module often involves the Rho family GTPases Cdc42 and Rac. The JNK module plays an important role in apoptosis, inflammation, cytokine production, and metabolism. Landmark discoveries in the area of JNK research Landmark discoveries in the area of JNK research are summarized in Figure 1.įigure 1. The c-Jun N-terminal kinases (JNKs) were first described in the early 1990s. The JNK pathway has been implicated in the mitogen activated protein kinase (MAPK) signaling in cardiac hypertrophy.Phosphorylation of the transcription factor p53.JNK pathway contributes to the control of a large number of cellular processes: The JNK pathway can also be activated through G protein-coupled receptors (GPCRs) using G proteins such as G12/13. This complexity is evident by the fact that there are 13 MAPK kinase kinases (MAPKKKs) responsible for feeding information into the JNK pathway. The JNK pathway is activated by a bewildering number of mechanisms. The pathway takes its name from the c-Jun N-terminal kinases 1–3 (JNK1–JNK3), which are the MAPKs that interact with the final effectors. It functions in the control of a number of cellular processes, including proliferation, embryonic development and apoptosis. The c-Jun N-terminal kinase (JNK) pathway is one of the major signaling cassettes of the mitogen-activated protein kinase (MAPK) signaling pathway. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |