Part of the MAPK family, c-Jun N-terminal kinases, or JNKs, respond to inflammatory cytokines, growth factors, and other cellular stress. JNK signaling is activated through receptor tyrosine kinases or G-coupled protein receptors which initiate a signaling cascade. Activation of these receptors results in phosphorylation and subsequent activation of a series of kinases, including Rho family members, like Rac and CDC42, MLKs, and MEKKs. Ultimately, these kinases phosphorylate MKK4 and MKK7 which activate JNK proteins. Next, JNK proteins translocate to the nucleus where they interact with transcription factors including c-Jun and p53 to modulate gene expression resulting in apoptosis, cell migration, proliferation, or inflammation.
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