AI Article Synopsis
- Cyclin G1 is a gene responsive to p53 and is induced in cells under ARF arrest, but its function in growth regulation is not fully understood.
- Cyclin G1 interacts with ARF, Mdm2, and p53 and can induce a halt in G(1)-phase cell growth at high levels, linked to p53 activation.
- While high levels of cyclin G1 inhibit growth, lower levels can enhance ARF's growth arrest effect, and its regulation involves degradation by Mdm2, indicating a complex role in tumor suppression pathways involving p53 and pRb.
Article Abstract
Cyclin G1 is a p53-responsive gene that is induced in alternative reading frame (ARF)-arrested cells, yet its role in growth control is unclear. We tested its effects on growth and involvement in the ARF-Mdm2-p53 tumor suppressor pathway. We show that cyclin G1 interacts with ARF, Mdm2, and p53 in vitro and in vivo. At high levels, cyclin G1 induces a G(1)-phase arrest in mammalian cells that coincides with p53 activation. Conversely, lower levels of cyclin G1 lack intrinsic growth inhibitory effects yet potentiate ARF-mediated growth arrest. Notably, cyclin G1 is down-regulated by Mdm2 through proteasome-mediated degradation. These data suggest that cyclin G1 is a positive feedback regulator of p53 whose expression is restrained by Mdm2. Interestingly, growth inhibition by cyclin G1 does not require p53 but instead exhibits partial retinoblastoma protein (pRb) dependence. These findings reveal that cyclin G1 has growth inhibitory activity that is mechanistically linked to ARF-p53 and pRb tumor suppressor pathways.
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