ArticleMolecular and cellular biology2006
FAT10/diubiquitin-like protein-deficient mice exhibit minimal phenotypic differences.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
61 citing papers in PubMed, 97 citations in OpenAlex.
- Review
- NUB1 traps unfolded FAT10 for ubiquitin-independent degradation by the 26S proteasome.Nature structural & molecular biology · 2025Article
- Cas12a-knock-in mice for multiplexed genome editing, disease modelling and immune-cell engineering.Nature biomedical engineering · 2025Article
- Molecular choreography of E1 enzymes in ubiquitin-like protein cascades: New insights into dynamics and specificity.The Journal of biological chemistry · 2025Review
- Ubiquitin-like Proteins in Autoimmune Diseases: Current Evidence and Therapeutic Opportunities.Immune network · 2025Review
- Identifying disease progression biomarkers in metabolic associated steatotic liver disease (MASLD) through weighted gene co-expression network analysis and machine learning.Journal of translational medicine · 2025Article
- Article
- The ubiquitin-like modifier FAT10 is not essential for MHC-I antigen presentation.Frontiers in immunology · 2025Article
- Phosphorylated FAT10 Is More Efficiently Conjugated to Substrates, Does Not Bind to NUB1L, and Does Not Alter Degradation by the Proteasome.Biomedicines · 2024Article
- UBDP1 pseudogene and UBD network competitively bind miR‑6072 to promote glioma progression.International journal of oncology · 2024Article
- Tumor necrosis factor mediates USE1-independent FAT10ylation under inflammatory conditions.Life science alliance · 2023Article
- The ubiquitin-like modifier FAT10 covalently modifies HUWE1 and strengthens the interaction of AMBRA1 and HUWE1.PloS one · 2023Article
- UBA6 and NDFIP1 regulate the degradation of ferroportin.Haematologica · 2022Article
- FAT10 is a Prognostic Biomarker and Correlated With Immune Infiltrates in Skin Cutaneous Melanoma.Frontiers in molecular biosciences · 2022Article
- The ubiquitin-like modifier FAT10 inhibits retinal PDE6 activity and mediates its proteasomal degradation.The Journal of biological chemistry · 2020Article
- The Role of FAT10 in Alcoholic Hepatitis Pathogenesis.Biomedicines · 2020Review
- Regulation of Interferon Induction by the Ubiquitin-Like Modifier FAT10.Biomolecules · 2020Review
- Post-translational modification and protein sorting to small extracellular vesicles including exosomes by ubiquitin and UBLs.Cellular and molecular life sciences : CMLS · 2019Review
- The ubiquitin-like modifier FAT10 interferes with SUMO activation.Nature communications · 2019Article
- UBA6 and Its Bispecific Pathways for Ubiquitin and FAT10.International journal of molecular sciences · 2019Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The FAT10 gene encodes a diubiquitin-like protein containing two tandem head-to-tail ubiquitin-like domains. There is a high degree of similarity between murine and human FAT10 sequences at both the mRNA and protein levels. In various cell lines, FAT10 expression was shown to be induced by gamma interferon or by tumor necrosis factor alpha. In addition, FAT10 expression was found to be up-regulated in some Epstein-Barr virus-infected B-cell lines, in activated dendritic cells, and in several epithelial tumors. However, forced expression of FAT10 in cultured cells was also found to produce apoptotic cell death. Overall, these findings suggest that FAT10 may modulate cellular growth or cellular viability. Here we describe the steps to generate, by genetic targeting, a FAT10 gene knockout mouse model. The FAT10 knockout homozygous mice are viable and fertile. No gross lesions or obvious histological differences were found in these mutated mice. Examination of lymphocyte populations from spleen, thymus, and bone marrow did not reveal any abnormalities. However, flow cytometry analysis demonstrated that the lymphocytes of FAT10 knockout mice were, on average, more prone to spontaneous apoptotic death. Physiologically, these mice demonstrated a high level of sensitivity toward endotoxin challenge. These findings indicate that FAT10 may function as a survival factor.
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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.