ArticleThe Journal of biological chemistry2015
NEDD8 Ultimate Buster 1 Long (NUB1L) Protein Suppresses Atypical Neddylation and Promotes the Proteasomal Degradation of Misfolded Proteins.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Neddylation: from regulatory mechanisms to clinical implications in cancer.Journal of advanced research · 2026Review
- Deciphering the roles of neddylation modification in hepatocellular carcinoma: Molecular mechanisms and targeted therapeutics.Genes & diseases · 2025Review
- CBL-b E3 ligase-mediated neddylation and activation of PARP-1 induce vascular calcification.Experimental & molecular medicine · 2024Article
- Quantitative proteomics reveals cellular responses to individual mAb expression and tunicamycin in CHO cells.Applied microbiology and biotechnology · 2024Article
- Targeting NEDD8 suppresses surgical stress-facilitated metastasis of colon cancer via restraining regulatory T cells.Cell death & disease · 2024Article
- Neddylation is required for perinatal cardiac development through stimulation of metabolic maturation.Cell reports · 2023Article
- Article
- Signaling Pathways Involved in Myocardial Ischemia-Reperfusion Injury and Cardioprotection: A Systematic Review of Transcriptomic Studies inJournal of cardiovascular development and disease · 2022Review
- Role of VAPB and vesicular profiles in α-synuclein aggregates in multiple system atrophy.Brain pathology (Zurich, Switzerland) · 2021Article
- Review
- Stress-induced NEDDylation promotes cytosolic protein aggregation through HDAC6 in a p62-dependent manner.iScience · 2021Article
- Dysfunctional Mitochondrial Dynamic and Oxidative Phosphorylation Precedes Cardiac Dysfunction in R120G-αB-Crystallin-Induced Desmin-Related Cardiomyopathy.Journal of the American Heart Association · 2020Article
- Neddylation, an Emerging Mechanism Regulating Cardiac Development and Function.Frontiers in physiology · 2020Review
- The potential role of neddylation in pre- and postnatal cardiac remodeling.American journal of physiology. Heart and circulatory physiology · 2019Article
- Transient inhibition of neddylation at neonatal stage evokes reversible cardiomyopathy and predisposes the heart to isoproterenol-induced heart failure.American journal of physiology. Heart and circulatory physiology · 2019Article
- Non-Proteasomal UbL-UbA Family of Proteins in Neurodegeneration.International journal of molecular sciences · 2019Review
- NEDDylation promotes nuclear protein aggregation and protects the Ubiquitin Proteasome System upon proteotoxic stress.Nature communications · 2018Article
- Neddylation mediates ventricular chamber maturation through repression of Hippo signaling.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Systemic inhibition of neddylation by 3-day MLN4924 treatment regime does not impair autophagic flux in mouse hearts and brains.American journal of cardiovascular disease · 2017Article
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Neddylation is a posttranslational modification that controls diverse biological processes by covalently conjugating the ubiquitin-like protein NEDD8 to specific targets. Neddylation is commonly mediated by NEDD8-specific enzymes (typical neddylation) and, sometimes, by ubiquitin enzymes (atypical neddylation). Although typical neddylation is known to regulate protein function in many ways, the regulatory mechanisms and biological consequence of atypical neddylation remain largely unexplored. Here we report that NEDD8 conjugates were accumulated in the diseased hearts from mouse models and human patients. Proteotoxic stresses induced typical and atypical neddylation in cardiomyocytes. Loss of NUB1L exaggerated atypical neddylation, whereas NUB1L overexpression repressed atypical neddylation through promoting the degradation of NEDD8. Activation of atypical neddylation accumulated a surrogate misfolded protein, GFPu. In contrast, suppression of atypical neddylation by NUB1L overexpression enhanced GFPu degradation. Moreover, NUB1L depletion accumulated a cardiomyopathy-linked misfolded protein, CryAB(R120G), whereas NUB1L overexpression promoted its degradation through suppressing neddylation of ubiquitinated proteins in cardiomyocytes. Consequently, NUB1L protected cells from proteotoxic stress-induced cell injury. In summary, these data indicate that NUB1L suppresses atypical neddylation and promotes the degradation of misfolded proteins by the proteasome. Our findings also suggest that induction of NUB1L could potentially become a novel therapeutic strategy for diseases with increased proteotoxic stress.
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