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human homolog is a diubiquitin protein that may function in antigen processing and presentation [RGD, Feb 2006].. Additionally we are shipping UBD Antibodies (76) and UBD Proteins (19) and many more products for this protein.
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We also found that FAT10 may act its oncogenic functions through regulating HOXB9 (show HOXB9 ELISA Kits). Collectively, the results suggested that FAT10 may be a novel therapeutic target for osteosarcoma patients
High expression of FAT10 is associated with glioma.
Study demonstrates how the coordinated interplay of RIG-I (show DDX58 ELISA Kits), TRIM25 (show TRIM25 ELISA Kits), and FAT10 regulate the antiviral innate inflammatory response.
Data suggest that ubiquitin D (UBD) provides a negative feedback on cytokine-induced activation of the endoplasmic reticulum to nucleus signaling 1 (IRE1alpha (show ERN1 ELISA Kits))/c-Jun N-terminal kinase (JNK) pro-apoptotic pathway in cytokine-exposed beta cells.
FAT10 can induce malignant transformation as evidenced from the anchorage-independent growth as well as in vivo tumor-forming abilities of FAT10-overexpressing NeHepLxHT cells.
repertoire of peptides eluted from MHC class I molecules was influenced by FAT10 expression
FAT10 is the only ubiquitin-like modifier known to date which directly targets its hundreds of substrates for degradation by the proteasome. (Review)
Conjugation of the ubiquitin activating enzyme UBE1 (show UBA1 ELISA Kits) with the ubiquitin-like modifier FAT10 targets it for proteasomal degradation
the interaction of FAT10 with MAD2 (show MAD2L1 ELISA Kits) is a key mechanism underlying the promalignant property of FAT10
Results identified a novel HCC (show FAM126A ELISA Kits) regulatory circuit involving FAT10, beta-catenin (show CTNNB1 ELISA Kits)/TCF4 (show TCF4 ELISA Kits), and HOXB9 (show HOXB9 ELISA Kits), the dysfunction of which drives invasive and metastatic character in HCC (show FAM126A ELISA Kits).
IFNalpha induced FAT10 expression, which is suppressed by ethanol feeding in both HCV(+) and HCV(-) mice
transcription downregulation of the Ufm1 (show UFM1 ELISA Kits) and FAT10 conjugation system in liver Mallory-Denk bodies formation
observations suggest novel roles of FAT10 in immune metabolic regulation that impact aging and chronic disease
FAT10 protects cardiac myocytes against apoptosis.
FAT10 is essential to the induction of Mallory-Denk body formation in di-carbethoxydihydrocollidine fed mice.
FAT10 mediates NF-kappaB (show NFKB1 ELISA Kits) activation and may promote tubulointerstitial inflammation in chronic kidney diseases.
Immunohistochemical studies demonstrated increased FAT10 expression in a model of HIV-associated nephropathy.
These findings indicate that FAT10 may function as a survival factor.
The link between Mallory Denk Body formation and neoplasia formation was likely due to the over expression of UBD (also called FAT10), which is up regulated in 90% of human hepatocellular carcinomas.
human homolog is a diubiquitin protein that may function in antigen processing and presentation
, ubiquitin-like protein FAT10