ArticleBiochemical and biophysical research communications2014
IKK-β/NF-κB p65 mediates p27(Kip1) protein degradation in arsenite response.
Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 7 citations in OpenAlex.
- SKP2 Regulates Pulmonary Inflammatory Injury Triggered by Bacterial Infection Through p27-Mediated Degradation of FOXN3.MedComm · 2026Article
- KCTD15 Is Overexpressed in her2+ Positive Breast Cancer Patients and Its Silencing Attenuates Proliferation in SKBR3 CELL LINE.Diagnostics (Basel, Switzerland) · 2022Article
- The RING domain in the anti-apoptotic protein XIAP stabilizes c-Myc protein and preserves anchorage-independent growth of bladder cancer cells.The Journal of biological chemistry · 2019Article
- ISO, via Upregulating MiR-137 Transcription, Inhibits GSK3β-HSP70-MMP-2 Axis, Resulting in Attenuating Urothelial Cancer Invasion.Molecular therapy. Nucleic acids · 2018Article
- p27 kip1 haplo-insufficiency improves cardiac function in early-stages of myocardial infarction by protecting myocardium and increasing angiogenesis by promoting IKK activation.Scientific reports · 2014Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
p27(Kip1) is a potent inhibitor of the cyclin-dependent kinases that drive G1 to S phase transition. Since deregulation of p27(Kip1) is found in many malignancies and is associated with the poor prognosis, elucidation of the molecular bases for regulation of p27(Kip1) expression is of great significance, not only in providing insight into the understanding of biological p27(Kip1), but also in the development of new cancer therapeutic tactics. We here explored the inhibitory regulation of IKKβ on p27(Kip1) expression following arsenite exposure. We found that although the basal level of p27(Kip1) expression in the IKKβ(-/-) cells is much lower than that in the IKKβ(+/+) cells, the deletion of IKKβ in the MEFs led to a marked increase in p27(Kip1) protein induction due to arsenite exposure in comparison to that in the IKKβ(+/+) cells. The IKKβ regulatory effect on p27(Kip1) expression was also verified in the IKKβ(-/-) and IKKβ(-/-) cells with IKKβ reconstitutional expression, IKKβ(-/-) (IKKβ). Further studies indicated that IKKβ-mediated p27(Kip1) downregulation occurred at protein degradation level via p65-dependent and p50-independent manner. Moreover, the results obtained from the comparison of arsenite-induced GSK3β activation among transfectants of WT, IKKβ(-/-) and IKKβ(-/-) (IKKβ), and the utilization of GSKβ shRNA, demonstrated that IKKβ regulation of p27 protein degradation was mediated by GSK3β following arsenite exposure.
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