Ask about this productRelated genes to: USP33 antibody
- Gene:
- USP33 NIH gene
- Name:
- ubiquitin specific peptidase 33
- Previous symbol:
- -
- Synonyms:
- KIAA1097, VDU1
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-04
- Date modifiied:
- 2016-10-05
Related products to: USP33 antibody
Related articles to: USP33 antibody
- The ubiquitin-specific proteases (USPs) family is the largest family of human deubiquitinating enzymes (DUBs). While most USPs are agnostic to polyubiquitin linkage-type, their substrate specificity is thought to be mediated by the recognition of the ubiquitnated protein itself. In addition to their catalytic domain, USPs have one or more auxiliary domains (ADs) with key functions in regulating DUB activity and localization. We hypothesize that some ADs bind short linear motifs (SLiMs) typically found in intrinsically disordered regions of proteins to achieve targeting to substrates and multiprotein complexes. To test this, we systematically assess the potential of 29 USP-ADs and two full-length USPs for SLiM binding using a combination of proteomic-peptide phage display, peptide SPOT arrays and affinity measurements. We discover SLiM-based interactions for 14 ADs from 9 USP-DUBs, including CYLD, USP11, USP19, USP20, USP22 and USP33, and define the consensus motif and properties of the SLiM-AD binding. Interestingly, we establish that the zf-UBP and DUSP2 domains of USP20 and USP33 are SLiM binding ADs with similar binding profiles, explaining the functional redundancy between the two DUBs. Our work reveals unique motifs recognized by the auxiliary domains CAP-Gly, UBL, zf-UBP and DUSP, with potential functional implications for substrate recognition and complex assemblies. - Source: PubMed
Publication date: 2026/05/18
Konstantinou AimilianiCórdova-Pérez AliciaVarga Julia KMadhu PriyankaSimonetti LeandroVieler MaximilianIshimura RyosukeLamoliatte FredericSchueler-Furman OraDavey Norman EKulathu YogeshIvarsson Ylva - Lenvatinib resistance represents a primary cause of treatment failure in patients with advanced hepatocellular carcinoma (HCC), while its underlying molecular mechanisms remain incompletely understood. Using a CRISPR knockout library targeting human ubiquitination-related proteins, we identified ubiquitin-specific protease 33 (USP33) as a key factor of lenvatinib resistance in HCC. Transcriptome sequencing further demonstrated that USP33 induces epithelial-mesenchymal transition (EMT), and its downregulation suppresses EMT and enhances lenvatinib sensitivity in HCC cells. Through proteomic analysis, we identified interleukin-like EMT-inducing factor (ILEI) as a downstream target regulated by USP33 in this process. Mechanistically, USP33 functions as a deubiquitinase for eukaryotic translation elongation factor 1alpha 1 (eEF1A1), inhibiting its ubiquitin-mediated degradation and enhancing its protein stability, thereby promoting ILEI protein synthesis. Together, these findings reveal the significant role of the USP33/eEF1A1/ILEI axis in contributing to EMT and lenvatinib resistance, offering potential therapeutic targets and a rationale for strategies to overcome lenvatinib resistance in HCC. - Source: PubMed
Publication date: 2026/05/16
Lu HongchengHu GuohuiHuang ZhiHaoWang NingXie FeiHan DongchengGe Jin - An individual's host genetics influence its susceptibility to both COVID-19 and coronary artery disease (CAD). We analyzed large-scale GWAS datasets encompassing 7.7 million SNPs to identify shared genetic architecture between the two diseases. We identified 24 pleiotropic risk loci for both COVID-19 and CAD, with three loci (1p31.1, 8p21.3, and 18q11.2) showing strong evidence for a single shared causal variant. Loci in the 8p21.3 and 18q11.2 regions showed a bidirectional causal association: COVID-19 to CAD or vice versa, while the 1p31.1 locus only showed a CAD to COVID-19 unilateral casual association in a Mendelian randomization analysis (GSMR). A fine mapping analysis of the three loci identified three lead pleiotropic variants (rs7515509, rs8192330, and rs4800403). The variant rs7515509 was spatially associated with , and ; rs8192330 with , and several other genes; and rs4800403 with and . Transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) from COVID-19 patients validated proxitropic variants (rs8192330 and rs4800403) with distinct expression signatures and prioritized and as the likely causal genes. Overexpression of has been linked to the heme metabolism hallmark, disrupted iron distribution in COVID-19 patients with comorbid CAD, and subsequent stress erythropoiesis, oxidative stress, immunological dysfunction, and altered wound healing, while a lower expression of has been observed in the cytoplasmic translation and regulation of mRNA metabolism. In conclusion, we identified shared genetic components for COVID-19 and CAD and prioritized and as the likely causal genes for the observed shared genetic risk. COVID-19 may act as an acute stressor that unmask or accelerates underlying CAD. - Source: PubMed
Publication date: 2026/05/05
Ali Muhammad SarfrazHaider WaseemAziz SanaMohammad AnwaruddinManichaikul AniShi Weibin - Deubiquitination(DUB) is a critical cellular process that regulates protein stability and functionality, playing essential roles in cell proliferation, migration, tumorigenesis, and various molecular signaling pathways. Within the DUB enzyme family, ubiquitin-specific protease 33 (USP33) is found to be aberrantly expressed in several cancers, including a significant reduction in colorectal cancer (CRC) tissues. The decreased expression of USP33 impairs its ability to inhibit CRC cell proliferation, migration, and invasion, potentially through its involvement in key signaling pathways such as the β-arrestin-dependent ERK pathway, Slit-Robo pathway, and Wnt/β-catenin pathway. This review highlights the interaction between USP33 and these signaling pathways, exploring its potential as a novel independent prognostic biomarker for CRC and its promise as a therapeutic target. - Source: PubMed
Publication date: 2026/02/09
Dai YuLuo XinyuWu HengLuo YajunDeng ZijianWu JiqiangZhang LiYan Jin - This study aimed to investigate the mechanism of the involvement of USP33 in autophagic ferroptosis in endometriosis (EMs). - Source: PubMed
Publication date: 2025/12/26
Li LiYou WuZhang Mingzhe