Members of the MAPK family, the c-Jun N-terminal kinases (JNKs) are activated by environmental stresses and inflammatory cytokines. Ten JNK isoforms are created by alternative splicing of mRNA transcripts derived from three genes: JNK1, JNK2, and JNK3. All JNKs are activated by dual phosphorylation; at T183/Y185 for JNK1 and 2, and T221/Y223 for JNK3. Activated JNKs translocate to the nucleus where they regulate the activity of several transcription factors; including the c-Jun component of AP-1 and ATF-2.