ArticlePloS one2013
The TBC1D15 oncoprotein controls stem cell self-renewal through destabilization of the Numb-p53 complex.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Prognostic Value of TBC1D1 and Its Relationship With the Tumor Microenvironment in Pancreatic Cancer: A Study Based on Single-Cell Sequencing.FASEB bioAdvances · 2025Article
- NOTCH localizes to mitochondria through the TBC1D15-FIS1 interaction and is stabilized via blockade of E3 ligase and CDK8 recruitment to reprogram tumor-initiating cells.Experimental & molecular medicine · 2024Article
- Article
- Aberrant phosphorylation inactivates Numb in breast cancer causing expansion of the stem cell pool.The Journal of cell biology · 2022Article
- Review
- Identification of key gene signatures for the overall survival of ovarian cancer.Journal of ovarian research · 2022Article
- HCV and tumor-initiating stem-like cells.Frontiers in physiology · 2022Review
- Atypical Rearrangements in APL-Like Acute Myeloid Leukemias: Molecular Characterization and Prognosis.Frontiers in oncology · 2022Review
- Model-based analysis uncovers mutations altering autophagy selectivity in human cancer.Nature communications · 2021Article
- A community effort to identify and correct mislabeled samples in proteogenomic studies.Patterns (New York, N.Y.) · 2021Article
- p53 destabilizing protein skews asymmetric division and enhances NOTCH activation to direct self-renewal of TICs.Nature communications · 2020Article
- TBC1D15/RAB7-regulated mitochondria-lysosome interaction confers cardioprotection against acute myocardial infarction-induced cardiac injury.Theranostics · 2020Article
- A fragment activity assay reveals the key residues of TBC1D15 GTPase-activating protein (GAP) in Chiloscyllium plagiosum.BMC molecular biology · 2019Article
- Proteomic screening identifies the zonula occludens protein ZO-1 as a new partner for ADAM12 in invadopodia-like structures.Oncotarget · 2018Article
- Regulation of Mitochondrial Dynamics by Proteolytic Processing and Protein Turnover.Antioxidants (Basel, Switzerland) · 2018Review
- Crystal structure of TBC1D15 GTPase-activating protein (GAP) domain and its activity on Rab GTPases.Protein science : a publication of the Protein Society · 2017Article
- G-actin guides p53 nuclear transport: potential contribution of monomeric actin in altered localization of mutant p53.Scientific reports · 2016Article
- A New Member of the TBC1D15 Family from Chiloscyllium plagiosum: Rab GTPase-Activating Protein Based on Rab7 as a Substrate.Marine drugs · 2015Article
- Silencing of TBC1D15 promotes RhoA activation and membrane blebbing.Molecular and cellular biochemistry · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Stem cell populations are maintained through self-renewing divisions in which one daughter cell commits to a specific fate while the other retains the multipotent characteristics of its parent. The p53 tumor suppressor, in conjunction with its interacting partner protein Numb, preserves this asymmetry and functions as a vital barrier against the unchecked expansion of tumor stem cell pools; however, little is known about the biological control of the Numb-p53 interaction. We show here that Numb and p53 are the constituents of a high molecular mass complex, which is disintegrated upon activation of aPKCζ, a Numb kinase. Using large-scale affinity purification and tandem mass spectrometry, we identify TBC1D15 as a Numb-associated protein and demonstrate that its amino-terminal domain disengages p53 from Numb, triggering p53 proteolysis and promoting self-renewal and pluripotency. Cellular levels of TBC1D15 are diminished upon acute nutrient deprivation through autophagy-mediated degradation, indicating that TBC1D15 serves as a conduit through which cellular metabolic status is linked to self-renewal. The profound deregulation of TBC1D15 expression exhibited in a diverse array of patient tumors underscores its proposed function as an oncoprotein.
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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.