ArticleOncogene2007
Antizyme1 mediates AURKAIP1-dependent degradation of Aurora-A.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 74 citations in OpenAlex.
- Antizyme inhibitor family: biological and translational research implications.Cell communication and signaling : CCS · 2024Review
- Recent Updates on Oncogenic Signaling of Aurora Kinases in Chemosensitive, Chemoresistant Cancers: Novel Medicinal Chemistry Approaches for Targeting Aurora Kinases.Current medicinal chemistry · 2024Review
- AURKAIP1 actuates tumor progression through stabilizing DDX5 in triple negative breast cancer.Cell death & disease · 2023Article
- Review
- EPLIN-β is a novel substrate of ornithine decarboxylase antizyme 1 and mediates cellular migration.Journal of cell science · 2023Article
- Role of Polyamine-Induced Dimerization of Antizyme in Its Cellular Functions.International journal of molecular sciences · 2022Article
- Myocardin-related transcription factor and serum response factor regulate cilium turnover by both transcriptional and local mechanisms.iScience · 2021Article
- Targeting AURKA in Cancer: molecular mechanisms and opportunities for Cancer therapy.Molecular cancer · 2021Review
- Role of Antizyme Inhibitor Proteins in Cancers and Beyond.OncoTargets and therapy · 2021Review
- Pan-cancer driver copy number alterations identified by joint expression/CNA data analysis.Scientific reports · 2020Article
- Insights into the non-mitotic functions of Aurora kinase A: more than just cell division.Cellular and molecular life sciences : CMLS · 2020Review
- Critical Factors in Human Antizymes that Determine the Differential Binding, Inhibition, and Degradation of Human Ornithine Decarboxylase.Biomolecules · 2019Article
- Developing a novel FRET assay, targeting the binding between Antizyme-AZIN.Scientific reports · 2019Article
- The antizyme family for regulating polyamines.The Journal of biological chemistry · 2018Review
- Antizyme Inhibitors in Polyamine Metabolism and Beyond: Physiopathological Implications.Medical sciences (Basel, Switzerland) · 2018Review
- Novel ubiquitin-independent nucleolar c-Myc degradation pathway mediated by antizyme 2.Scientific reports · 2018Article
- Antizyme inhibitor 1: a potential carcinogenic molecule.Cancer science · 2017Review
- OAZ1 knockdown enhances viability and inhibits ER and LHR transcriptions of granulosa cells in geese.PloS one · 2017Article
- Ribosomal frameshifting and transcriptional slippage: From genetic steganography and cryptography to adventitious use.Nucleic acids research · 2016Review
- Multifaceted interactions and regulation between antizyme and its interacting proteins cyclin D1, ornithine decarboxylase and antizyme inhibitor.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of Aurora-A oncogene has been shown to induce genomic instability and tumorigenesis. Cellular levels of Aurora-A are regulated by multiple mechanisms including the proteasome-dependent degradation of Aurora-A protein. Cell-cycle-dependent turnover of Aurora-A protein is mediated by cdh1 through ubiquitin (Ub)- and proteasome-dependent pathway. However, Aurora-A kinase interacting protein 1 (AURKAIP1), a negative regulator of Aurora-A, also promotes proteasome-dependent Aurora-A degradation through an Ub-independent mechanism. In an attempt to understand how AURKAIP1 promotes Aurora-A degradation through Ub-independent pathway, we demonstrate here that antizyme1 (Az1), a well-studied mediator of Ub-independent protein degradation pathway, regulates Aurora-A protein stability. We show that ectopic or polyamine-induced expression of Az1 can lower the steady-state levels of Aurora-A. The effect of Az1 on Aurora-A turnover was shown to be proteasome-dependent, but Ub-independent. Az1 interacts with Aurora-A in vivo and the interaction between Aurora-A and Az1 is essential for the Az1-mediated Aurora-A degradation. Furthermore, we observed that AURKAIP1 could not promote degradation of Aurora-A mutant, which is defective in Az1 interaction. Coexpression of the Az inhibitor (AzI), which downregulates Az1 functions, also abrogated AURKAIP1-mediated degradation of Aurora-A. We further demonstrated that AURKAIP1, Az1 and Aurora-A could exist as a ternary complex and AURKAIP1 enhances the interaction between Az1 and Aurora-A. We propose that AURKAIP1 might function upstream of the Az1 by enhancing the binding affinity of Az1 to Aurora-A to promote recognition, targeting to proteasome and subsequent degradation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.