ArticleOncogene2008
Antizyme, a mediator of ubiquitin-independent proteasomal degradation and its inhibitor localize to centrosomes and modulate centriole amplification.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Development of a Diagnostic Model for Focal Segmental Glomerulosclerosis: Integrating Machine Learning on Activated Pathways and Clinical Validation.International journal of general medicine · 2025Article
- Antizyme inhibitor family: biological and translational research implications.Cell communication and signaling : CCS · 2024Review
- Role of Antizyme Inhibitor Proteins in Cancers and Beyond.OncoTargets and therapy · 2021Review
- Antizyme Inhibitors in Polyamine Metabolism and Beyond: Physiopathological Implications.Medical sciences (Basel, Switzerland) · 2018Review
- 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
- The benefits of local depletion: The centrosome as a scaffold for ubiquitin-proteasome-mediated degradation.Cell cycle (Georgetown, Tex.) · 2016Review
- A role for antizyme inhibitor in cell proliferation.Amino acids · 2015Article
- Phosphorylation of Mps1 by BRAFV600E prevents Mps1 degradation and contributes to chromosome instability in melanoma.Oncogene · 2013Article
- Recoding RNA editing of AZIN1 predisposes to hepatocellular carcinoma.Nature medicine · 2013Article
- Centrosome dysfunction contributes to chromosome instability, chromoanagenesis, and genome reprograming in cancer.Frontiers in oncology · 2013Review
- Knockdown of antizyme inhibitor decreases prostate tumor growth in vivo.Amino acids · 2012Article
- Article
- Evidence of a role for antizyme and antizyme inhibitor as regulators of human cancer.Molecular cancer research : MCR · 2011Review
- Centriole assembly and the role of Mps1: defensible or dispensable?Cell division · 2011Article
- Antizyme restrains centrosome amplification by regulating the accumulation of Mps1 at centrosomes.Molecular biology of the cell · 2010Article
- Recurrent emergence of catalytically inactive ornithine decarboxylase homologous forms that likely have regulatory function.Journal of molecular evolution · 2010Article
- Expression of antizyme inhibitor 2 in mast cells and role of polyamines as selective regulators of serotonin secretion.PloS one · 2009Article
- Antizyme and antizyme inhibitor, a regulatory tango.Cellular and molecular life sciences : CMLS · 2009Review
- When 2+2=5: the origins and fates of aneuploid and tetraploid cells.Biochimica et biophysica acta · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The potential tumor suppressor antizyme and its endogenous inhibitor (antizyme inhibitor, AZI) have been implicated in the ubiquitin-independent proteasomal degradation of proteins involved in cell proliferation as well as in the regulation of polyamine levels. We show here that both antizyme and AZI concentrate at centrosomes and that antizyme preferentially associates with the maternal centriole. Interestingly, alterations in the levels of these proteins have opposing effects on centrosomes. Depletion of antizyme in various cell lines and primary cells leads to centrosome overduplication, whereas overexpression of antizyme reduces numerical centrosome abnormalities. Conversely, silencing of the antizyme inhibitor, AZI, results in a decrease of numerical centrosome abnormalities, whereas overexpression of AZI leads to centrosome overduplication. We further show that the numerical centrosome abnormalities are due to daughter centriole amplification. In summary, our results demonstrate that alterations in the antizyme/AZI balance cause numerical centrosomal defects and suggest a role for ubiquitin-independent proteasomal degradation in centrosome duplication.
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Registered trials
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.