ArticleJournal of cell science2014
PML isoforms in response to arsenic: high-resolution analysis of PML body structure and degradation.
Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Twisting the End Game: How Telomere Chromatin Modifications Shape Telomere Maintenance.Aging cell · 2026Review
- PML mutants from arsenic-resistant patients reveal SUMO1-TOPORS and SUMO2/3-RNF4 degradation pathways.The Journal of cell biology · 2025Article
- Orphan nuclear receptors-induced ALT-associated PML bodies are targets for ALT inhibition.Nucleic acids research · 2024Article
- On the Prevalence and Roles of Proteins Undergoing Liquid-Liquid Phase Separation in the Biogenesis of PML-Bodies.Biomolecules · 2023Article
- PML Body Biogenesis: A Delicate Balance of Interactions.International journal of molecular sciences · 2023Review
- Two-dimensional molecular condensation in cell signaling and mechanosensing.Acta biochimica et biophysica Sinica · 2023Review
- Reorganization of Cell Compartmentalization Induced by Stress.Biomolecules · 2022Review
- Zinc controls PML nuclear body formation through regulation of a paralog specific auto-inhibition in SUMO1.Nucleic acids research · 2022Article
- New Evidence of the Importance of Weak Interactions in the Formation of PML-Bodies.International journal of molecular sciences · 2022Article
- Effects of arsenic on the topology and solubility of promyelocytic leukemia (PML)-nuclear bodies.PloS one · 2022Article
- TRAIL-receptor 2-a novel negative regulator of p53.Cell death & disease · 2021Article
- The Role of Non-Specific Interactions in Canonical and ALT-Associated PML-Bodies Formation and Dynamics.International journal of molecular sciences · 2021Article
- Superresolution light microscopy of theMolecular biology of the cell · 2021Article
- Photobody Detection Using Immunofluorescence and Super-Resolution Imaging in Arabidopsis.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Regulation of eIF2α by RNF4 Promotes Melanoma Tumorigenesis and Therapy Resistance.The Journal of investigative dermatology · 2020Article
- Functional 3D architecture in an intrinsically disordered E3 ligase domain facilitates ubiquitin transfer.Nature communications · 2020Article
- Arkadia/RNF111 is a SUMO-targeted ubiquitin ligase with preference for substrates marked with SUMO1-capped SUMO2/3 chain.Nature communications · 2019Article
- Visualizing ubiquitination in mammalian cells.EMBO reports · 2019Review
- Generation of specific inhibitors of SUMO-1- and SUMO-2/3-mediated protein-protein interactions using Affimer (Adhiron) technology.Science signaling · 2017Article
- Ataxia telangiectasia and rad3 related (ATR)-promyelocytic leukemia protein (PML) pathway of the DNA damage response in the brain of rats administered arsenic trioxide.Journal of toxicologic pathology · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Arsenic is a clinically effective treatment for acute promyelocytic leukaemia (APL) in which the promyelocytic leukaemia (PML) protein is fused to retinoic receptor alpha (RARα). PML-RARα is degraded by the proteasome by a SUMO-dependent, ubiquitin-mediated pathway in response to arsenic treatment, curing the disease. Six major PML isoforms are expressed as a result of alternative splicing, each of which encodes a unique C-terminal region. Using a system in which only a single EYFP-linked PML isoform is expressed, we demonstrate that PMLI, PMLII and PMLVI accumulate in the cytoplasm following arsenic treatment, whereas PMLIII, PMLIV and PMLV do not. 3D structured illumination was used to obtain super-resolution images of PML bodies, revealing spherical shells of PML along with associated SUMO. Arsenic treatment results in dramatic isoform-specific changes to PML body ultrastructure. After extended arsenic treatment most PML isoforms are degraded, leaving SUMO at the core of the nuclear bodies. A high-content imaging assay identifies PMLV as the isoform most readily degraded following arsenic treatment, and PMLIV as relatively resistant to degradation. Immunoprecipitation analysis demonstrates that all PML isoforms are modified by SUMO and ubiquitin after arsenic treatment, and by using siRNA, we demonstrate that arsenic-induced degradation of all PML isoforms is dependent on the ubiquitin E3 ligase RNF4. Intriguingly, depletion of RNF4 results in marked accumulation of PMLV, suggesting that this isoform is an optimal substrate for RNF4. Thus the variable C-terminal domain influences the rate and location of degradation of PML isoforms following arsenic treatment.
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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.