ArticleCell cycle (Georgetown, Tex.)2013
The deubiquitylase USP15 stabilizes newly synthesized REST and rescues its expression at mitotic exit.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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32 citing papers in PubMed, 48 citations in OpenAlex.
- Key roles of ubiquitination in regulating critical regulators of cancer stem cell functionality.Genes & diseases · 2025Review
- RAPIDASH: Tag-free enrichment of ribosome-associated proteins reveals composition dynamics in embryonic tissue, cancer cells, and macrophages.Molecular cell · 2024Article
- Ectopic USP15 expression inhibits HIV-1 transcription involving changes in YY1 deubiquitination and stability.Frontiers in cellular and infection microbiology · 2024Article
- RAPIDASH: A tag-free enrichment of ribosome-associated proteins reveals compositional dynamics in embryonic tissues and stimulated macrophages.bioRxiv : the preprint server for biology · 2023Article
- CRISPR/Cas9-based genome-wide screening of the deubiquitinase subfamily identifies USP3 as a protein stabilizer of REST blocking neuronal differentiation and promotes neuroblastoma tumorigenesis.Journal of experimental & clinical cancer research : CR · 2023Article
- Transcription factor network analysis identifies REST/NRSF as an intrinsic regulator of CNS regeneration in mice.Nature communications · 2022Article
- USP33 deubiquitinates and stabilizes HIF-2alpha to promote hypoxia response in glioma stem cells.The EMBO journal · 2022Article
- USP15 in Cancer and Other Diseases: From Diverse Functionsto Therapeutic Targets.Biomedicines · 2022Review
- USP15 and USP4 facilitate lung cancer cell proliferation by regulating the alternative splicing of SRSF1.Cell death discovery · 2022Article
- A flexible microfluidic system for single-cell transcriptome profiling elucidates phased transcriptional regulators of cell cycle.Scientific reports · 2021Article
- Selective autophagy as a therapeutic target for neurological diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Post-Translational Modifications of Deubiquitinating Enzymes: Expanding the Ubiquitin Code.Frontiers in pharmacology · 2021Review
- Advances in Deubiquitinating Enzyme Inhibition and Applications in Cancer Therapeutics.Cancers · 2020Review
- Regulation of Deubiquitinating Enzymes by Post-Translational Modifications.International journal of molecular sciences · 2020Review
- TIFAB Regulates USP15-Mediated p53 Signaling during Stressed and Malignant Hematopoiesis.Cell reports · 2020Article
- DUBbing Down Translation: The Functional Interaction of Deubiquitinases with the Translational Machinery.Molecular cancer therapeutics · 2019Review
- Transcriptional repressor REST drives lineage stage-specific chromatin compaction atScience signaling · 2019Article
- The structure of the deubiquitinase USP15 reveals a misaligned catalytic triad and an open ubiquitin-binding channel.The Journal of biological chemistry · 2018Article
- The deubiquitylase USP15 regulates topoisomerase II alpha to maintain genome integrity.Oncogene · 2018Article
- Ubiquitin Specific Peptidase 15 (USP15) suppresses glioblastoma cell growth via stabilization of HECTD1 E3 ligase attenuating WNT pathway activity.Oncotarget · 2017Article
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7 authors at 1 institution in 1 country.
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Abstract
Reversible ubiquitylation of proteins contributes to their integrity, abundance and activity. The RE1-silencing transcription factor (REST) plays key physiological roles and is dysregulated in a spectrum of disease. It is rapidly turned over and is phosphorylated, polyubiquitylated and degraded en masse during neuronal differentiation and cell cycle progression. Through siRNA screening we identified the deubiquitylase USP15 as a key regulator of cellular REST. Both antagonism of REST polyubiquitylation and rescue of endogenous REST levels are dependent on the deubiquitylase activity of USP15. However, USP15 depletion does not destabilize pre-existing REST, but rather specifically impairs de novo REST synthesis. Indeed, we find that a small fraction of endogenous USP15 is associated with polysomes. In accordance with these findings, USP15 does not antagonize the degradation of phosphorylated REST at mitosis. Instead it is required for the rapid accumulation of newly synthesized REST on mitotic exit, thus playing a key role in its cell cycle oscillations. Importantly, this study reveals a novel role for a DUB in specifically promoting new protein synthesis.
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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.