
-   Activation of c-Jun via JNK signaling contributes to stress-induced cell death in a variety of cell types. For example, treatment of Jurkat T cell line with UV, gamma irradiation, or anisomycin lead to prolonged JNK activation in parallel with FasL expression and cell death, indicating that FasL might be downstream target of c-Jun [PMID: 9551965]. Activation of c-Jun in sympathetic neurons in the absence of nerve growth factor (NGF) leads to cell death mediated by BIM(EL), a proapoptotic BCL-2 family member [PMID: 11301023].
-   In human fibroblasts c-Jun promotes survival by negatively regulating the tumor-suppressor PTEN which leads to the activation of the Akt survival pathway [PMID: 16676006]. In human endothelial cells and mouse fibroblasts formation of c-Jun-ATF2 complex leads to activation of anti-apoptotic Bcl-XL protein [PMID: 20507983].
-   Transforming growth factor beta 1 (TGF-beta 1) and razoxane induced maximal c-jun mRNA expression in human keratinocytes 4 days after treatment, concurrent with predifferentiation growth arrest (PGA). TGF-beta 1 maintained high c-jun mRNA levels even after 3 more days, indicating stable induction [PMID: 1419906].
-   In JB6 cells, c-Jun mRNA expression was downregulated when cells entered a quiescent state due to reduced serum concentration. However, treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulated c-Jun expression and morphological changes, with varying expression levels in transformed cell foci [PMID: 7955078].

## Summary

The Jun gene, encoding the c-Jun protein, is a transcription factor that binds to the AP-1 consensus motif, modulating gene expression crucial for cell proliferation, differentiation, and apoptosis [CS: 9]. During conditions of stress or toxicity, such as UV exposure in skin, the upregulation of Jun enhances the transcriptional activity of AP-1 complexes that regulate genes responsible for cell survival and apoptosis [CS: 8]. For example, in fibroblasts c-Jun can promote cell survival through its negative regulation of tumor suppressor PTEN, leading to activation of the Akt pathway, which could serve as a defense mechanism against further damage [CS: 7].

In T-cells damaged with UV, gamma irradiation, or anisomycin, prolonged JNK activation leads to FasL expression and cell death, which may be a response to eliminate cells with potential UV-induced DNA damage [CS: 8].
