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Activator protein 1 transcription factor subunit c-Jun (c-Jun) is a DNA-binding protein encoded by the JUN gene and is a central component of the AP-1 (Activator Protein 1) transcription factor complex, often functioning as a heterodimer with c-Fos or other bZIP proteins[1][2][3][7]. c-Jun regulates the transcription of numerous genes involved in critical biological processes including cell cycle progression, apoptosis, proliferation, immune response, and neural repair. It plays a dual role in promoting cell survival/proliferation and protecting against or contributing to cell death depending on cellular context and stimuli, such as stress or cytokines[1][2][3][6][7]. Dysregulation of c-Jun is implicated in various cancers (where it acts as a proto-oncogene), inflammation, neurodegenerative diseases, and tissue injury responses[1][3][5][6][7]. Its transcriptional activity is tightly regulated by phosphorylation, primarily via the stress-activated JNK pathway, making upstream kinases and the AP-1/c-Jun axis a subject of therapeutic research[3][9]. No selective direct c-Jun inhibitors are currently in standard therapeutic use, but it remains a validated target for anti-cancer and anti-inflammatory drug development.
Modulation of AP-1-dependent gene transcription (antagonists/inhibitors) Inhibition of c-Jun N-terminal kinase (JNK) pathway to reduce c-Jun phosphorylation and activation[3][9]
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