ArticleOncogene2015
Deubiquitinating activity of CYLD is impaired by SUMOylation in neuroblastoma cells.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Targeting noncanonical nuclear factor kappa B signalling in CYLD cutaneous syndrome by selective inhibition of IκB kinase alpha.The British journal of dermatology · 2026Article
- Erasing marks: Functions of plant deubiquitylating enzymes in modulating the ubiquitin code.The Plant cell · 2024Review
- Targeting the ubiquitin-proteasome system: a novel therapeutic strategy for neuroblastoma.Frontiers in oncology · 2024Review
- CYLD in health and disease.Disease models & mechanisms · 2023Review
- 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
- Protein post-translational modifications in the regulation of cancer hallmarks.Cancer gene therapy · 2023Review
- FOSL1 promotes proneural-to-mesenchymal transition of glioblastoma stem cells via UBC9/CYLD/NF-κB axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Development of a prognostic model for children with neuroblastoma based on necroptosis-related genes.Frontiers in genetics · 2022Article
- Proteo-transcriptomics meta-analysis identifies SUMO2 as a promising target in glioblastoma multiforme therapeutics.Cancer cell international · 2021Article
- Deubiquitinating enzymes (DUBs): Regulation, homeostasis, and oxidative stress response.The Journal of biological chemistry · 2021Review
- Post-Translational Modifications of Deubiquitinating Enzymes: Expanding the Ubiquitin Code.Frontiers in pharmacology · 2021Review
- Proteomic Identification of an Endogenous Synaptic SUMOylome in the Developing Rat Brain.Frontiers in molecular neuroscience · 2021Article
- Regulation of Deubiquitinating Enzymes by Post-Translational Modifications.International journal of molecular sciences · 2020Review
- Epigenetic modifiers DNMT3A and BCOR are recurrently mutated in CYLD cutaneous syndrome.Nature communications · 2019Article
- The deubiquitinating enzyme UCHL1 is a favorable prognostic marker in neuroblastoma as it promotes neuronal differentiation.Journal of experimental & clinical cancer research : CR · 2018Article
- BAP1 induces cell death via interaction with 14-3-3 in neuroblastoma.Cell death & disease · 2018Article
- CYLD, A20 and OTULIN deubiquitinases in NF-κB signaling and cell death: so similar, yet so different.Cell death and differentiation · 2017Review
- Molecular basis for specificity of the Met1-linked polyubiquitin signal.Biochemical Society transactions · 2016Review
- MYCN promotes neuroblastoma malignancy by establishing a regulatory circuit with transcription factor AP4.Oncotarget · 2016Article
- Necroptosis: an alternative cell death program defending against cancer.Biochimica et biophysica acta · 2016Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CYLD is a deubiquitinating (DUB) enzyme that has a pivotal role in modulating nuclear factor kappa B (NF-κB) signaling pathways by removing the lysine 63- and linear-linked ubiquitin chain from substrates such as tumor necrosis factor receptor-associated factor 2 (TRAF2) and TRAF6. Loss of CYLD activity is associated with tumorigenicity, and levels of CYLD are lost or downregulated in different types of human tumors. In the present study, we found that high CYLD expression was associated with better overall survival and relapse-free neuroblastoma patient outcome, as well as inversely correlated with the stage of neuroblastoma. Retinoic acid-mediated differentiation of neuroblastoma restored CYLD expression and promoted SUMOylation of CYLD. This posttranslational modification inhibited deubiquitinase activity of CYLD against TRAF2 and TRAF6 and facilitated NF-κB signaling. Overexpression of non-SUMOylatable mutant CYLD in neuroblastoma cells reduced retinoic acid-induced NF-κB activation and differentiation of cells, but instead promoted cell death.
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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.