ArticleCellular and molecular life sciences : CMLS2012
The FAT10- and ubiquitin-dependent degradation machineries exhibit common and distinct requirements for MHC class I antigen presentation.
Article in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Intermolecular β-sheet Formation Guides the Interaction between Ubiquitin-like Modifier FAT10 and Adapter Protein NUB1L.Journal of the American Chemical Society · 2026Article
- Exploration of the mechanism by which Ubiquitin-like protein UBD promotes malignant progression of breast cancer.Medical oncology (Northwood, London, England) · 2026Article
- Multi-omics reveals FAT10 as an immunometabolic survival factor rewiring global metabolism in cancer.Cell communication and signaling : CCS · 2025Article
- NUB1 traps unfolded FAT10 for ubiquitin-independent degradation by the 26S proteasome.Nature structural & molecular biology · 2025Article
- The ubiquitin-like modifier FAT10 is not essential for MHC-I antigen presentation.Frontiers in immunology · 2025Article
- Article
- Human leukocyte antigen F-associated transcript 10 regulates thePhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
- The ubiquitin-like modifier FAT10 covalently modifies HUWE1 and strengthens the interaction of AMBRA1 and HUWE1.PloS one · 2023Article
- Ubiquitin like protein FAT10 repressed cardiac fibrosis after myocardial ischemic via mediating degradation of Smad3 dependent on FAT10-proteasome system.International journal of biological sciences · 2023Article
- Fast friends - Ubiquitin-like modifiers as engineered fusion partners.Seminars in cell & developmental biology · 2022Review
- Inhibition of UBA6 by inosine augments tumour immunogenicity and responses.Nature communications · 2022Article
- MLN4924 Inhibits Defective Ribosomal Product Antigen Presentation Independently of Direct NEDDylation of Protein Antigens.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- The case for FAT10 as a novel target in fatty liver diseases.Frontiers in pharmacology · 2022Review
- Identification and Verification of Necroptosis-Related Gene Signature With Prognosis and Tumor Immune Microenvironment in Ovarian Cancer.Frontiers in immunology · 2022Article
- Direct Conjugation of NEDD8 to the N-Terminus of a Model Protein Can Induce Degradation.Cells · 2021Article
- Ubiquitin-Like Protein UBD Promotes Cell Proliferation in Colorectal Cancer by Facilitating p53 Degradation.Frontiers in oncology · 2021Article
- The structure of the ubiquitin-like modifier FAT10 reveals an alternative targeting mechanism for proteasomal degradation.Nature communications · 2018Article
- The expression profile of the ubiquitin-like modifier FAT10 in immune cells suggests cell type-specific functions.Immunogenetics · 2018Article
- Prostaglandin EOncotarget · 2017Article
- De Novo Disruption of the Proteasome Regulatory Subunit PSMD12 Causes a Syndromic Neurodevelopmental Disorder.American journal of human genetics · 2017Article
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
Like ubiquitin (Ub), the ubiquitin-like protein FAT10 can serve as a signal for proteasome-dependent protein degradation. Here, we investigated the contribution of FAT10 substrate modification to MHC class I antigen presentation. We show that N-terminal modification of the human cytomegalovirus-derived pp65 antigen to FAT10 facilitates direct presentation and dendritic cell-mediated cross-presentation of the HLA-A2 restricted pp65(495-503) epitope. Interestingly, our data indicate that the pp65 presentation initiated by either FAT10 or Ub partially relied on the 19S proteasome subunit Rpn10 (S5a). However, FAT10 distinguished itself from Ub in that it promoted a pp65 response which was not influenced by immunoproteasomes or PA28. Further divergence occurred at the level of Ub-binding proteins with NUB1 supporting the pp65 presentation arising from FAT10, while it exerted no effect on that initiated by Ub. Collectively, our data establish FAT10 modification as a distinct and alternative signal for facilitated MHC class I antigen presentation.
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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.