| First Author | Meixner A | Year | 2010 |
| Journal | Cell Death Differ | Volume | 17 |
| Issue | 9 | Pages | 1409-19 |
| PubMed ID | 20300111 | Mgi Jnum | J:175212 |
| Mgi Id | MGI:5284967 | Doi | 10.1038/cdd.2010.22 |
| Citation | Meixner A, et al. (2010) Jun and JunD-dependent functions in cell proliferation and stress response. Cell Death Differ 17(9):1409-19 |
| abstractText | Jun is essential for fetal development, as fetuses lacking Jun die at mid-gestation with multiple cellular defects in liver and heart. Embryos expressing JunD in place of Jun (Jun(d/d)) can develop to term with normal fetal livers, but display cardiac defects as observed in fetuses lacking Jun. Jun(d/d) mouse embryonic fibroblasts (MEFs) exhibit early senescence, which can be rescued by EGF and HB-EGF stimulation, probably through activation of Akt signaling. Thus, JunD cannot functionally replace Jun in regulating fibroblast proliferation. In Jun(-/-) fetal livers, increased hydrogen peroxide levels are detected and expression of Nrf1 and Nrf2 (nuclear erythroid 2-related transcription factors) is downregulated. Importantly, increased oxidative stress as well as expression of Nrf1 and Nrf2 is rescued by JunD in Jun(d/d) fetal livers. These data show that Jun is of critical importance for cellular protection against oxidative stress in fetal livers and fibroblasts, and Jun-dependent cellular senescence can be restored by activation of the epidermal growth factor receptor pathway. |
