ArticleOncogene2007
TBP-1 protects the human oncosuppressor p14ARF from proteasomal degradation.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Unveiling a novel role for p19Arf (alternative reading frame) in mESC differentiation toward the pancreatic lineage.Scientific reports · 2026Article
- SUMOylation of the lysine-less tumor suppressor p14ARF counters ubiquitylation-dependent degradation.Cell death & disease · 2025Article
- PSMC3 promotes RNAi by maintaining AGO2 stability through USP14.Cellular & molecular biology letters · 2022Article
- Post-Translational Regulation of ARF: Perspective in Cancer.Biomolecules · 2020Review
- Dual Role of the Alternative Reading Frame ARF Protein in Cancer.Biomolecules · 2019Review
- PKC Dependent p14ARF Phosphorylation on Threonine 8 Drives Cell Proliferation.Scientific reports · 2018Article
- MDM2-mediated degradation of p14ARF: a novel mechanism to control ARF levels in cancer cells.PloS one · 2015Article
- Bacterial expression strategies for several Sus scrofa diacylglycerol kinase alpha constructs: solubility challenges.Scientific reports · 2013Article
- Mimicking p14ARF phosphorylation influences its ability to restrain cell proliferation.PloS one · 2013Article
- A 19S proteasomal subunit cooperates with an ERK MAPK-regulated degron to regulate accumulation of Fra-1 in tumour cells.Oncogene · 2012Article
- Proteasome inhibitors suppress expression of NPM and ARF proteins.Cell cycle (Georgetown, Tex.) · 2011Article
- A regulatory mechanism involving TBP-1/Tat-Binding Protein 1 and Akt/PKB in the control of cell proliferation.PloS one · 2011Article
- Tat-binding protein-1 (TBP-1), an ATPase of 19S regulatory particles of the 26S proteasome, enhances androgen receptor function in cooperation with TBP-1-interacting protein/Hop2.Endocrinology · 2009Article
- Residues in the alternative reading frame tumor suppressor that influence its stability and p53-independent activities.Experimental cell research · 2009Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The p14ARF tumor suppressor is a key regulator of cellular proliferation, frequently inactivated in human cancer. The mechanisms that regulate alternative reading frame (ARF) turnover have been obscure for long time, being ARF a relatively stable protein. Recently, it has been described that its degradation depends, at least in part, on the proteasome and that it can be subjected to N-terminal ubiquitination. We have previously reported that ARF protein levels are regulated by TBP-1 (Tat-Binding Protein 1), a multifunctional protein, component of the regulatory subunit of the proteasome, involved in different cellular processes. Here we demonstrate that the stabilization effect exerted by TBP-1 requires an intact N-terminal 39 amino acids in ARF and occurs independently from N-terminal ubiquitination of the protein. Furthermore, we observed that ARF can be degraded in vitro by the 20S proteasome, in the absence of ubiquitination and this effect can be counteracted by TBP-1. These observations seem relevant in the comprehension of the regulation of ARF metabolism as, among the plethora of cellular ARF's interactors already identified, only NPM/B23 and TBP-1 appear to be involved in the control of ARF intracellular levels.
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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.