Ask about this productRelated genes to: USP48 antibody
- Gene:
- USP48 NIH gene
- Name:
- ubiquitin specific peptidase 48
- Previous symbol:
- USP31
- Synonyms:
- FLJ23277, FLJ11328, FLJ20103, FLJ23054, MGC14879
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-29
- Date modifiied:
- 2015-08-26
Related products to: USP48 antibody
Related articles to: USP48 antibody
- The association between antiseizure medications (ASMs) and bone disorders remains inadequately investigated despite growing concern about drug-induced bone adverse events (AEs). We analyzed data from the FDA Adverse Event Reporting System (FAERS) database (Q1 2004-Q2 2025), identifying 7688 reports of bone health-related AEs listing ASMs as primary suspect drugs. Disproportionality analysis was performed using the reporting odds ratio (ROR) for signal detection. Subsequently, network pharmacology was applied to explore underlying biological pathways. Finally, two-sample Mendelian randomization (MR) was conducted to estimate potential causal associations between ASM-related gene targets and bone health outcomes. Disproportionality analysis revealed significant associations between ASMs and several bone health-related AEs, including increased blood alkaline phosphatase, ankle fracture, vitamin D deficiency, craniofacial fracture, cervical vertebral fracture, and skull fracture. Significant associations of bone health were identified for traditional enzyme-inducing ASMs, including carbamazepine, phenytoin, and phenobarbital, and newer agents, including perampanel, brivaracetam, lacosamide, and zonisamide. Pathway analysis predicted calcium and MAPK signaling. MR revealed genetically predicted effects of CAT, TNFRSF9, and USP48 on osteoporosis and of MGP, MFN2, PLOD1, and TNFRSF9 on ankle fracture. By integrating real-world pharmacovigilance with genetic insights, this study characterizes the associations between both conventional and newer ASMs and adverse bone health outcomes, mechanistically implicating the role of Calcium and MAPK signaling pathways. Furthermore, we identified several key regulatory genes. - Source: PubMed
Publication date: 2026/02/14
Gou ChenZhao QingqingHan Yanbing - Deubiquitinating enzymes (DUBs) are a class of biological macromolecules with molecular weights ranging from 30 to 150 kDa that play extensive roles in tumor initiation and progression. However, their implications in sorafenib resistance in liver cancer remain incompletely understood. In this study, we identified sorafenib resistance-associated DUBs through weighted gene co-expression network analysis and differential expression profiling. Subsequently, we developed a DUB-based predictive model for liver cancer resistance, designated ResiDUBs, using multivariate Cox regression analysis. This model was employed to assess drug resistance and prognostic outcomes. The ResiDUBs model-constructed based on five DUBs (OTUB1, USP32, USP48, USP49, and UBXN1)-stratified patients into high- and low-risk groups. Patients in the high-risk group exhibited significantly greater sorafenib resistance, poorer prognosis, and hyperactivation of the PI3K/AKT signaling pathway. Multi omics analyses, including single-cell RNA sequencing, spatial transcriptomics, and bulk RNA sequencing, consistently identified UBXN1 as the most prominent resistance-associated gene within the ResiDUBs signature. UBXN1 expression was markedly upregulated in treatment-resistant tumors. Knockdown of UBXN1 sensitizes liver cancer cells to sorafenib and inhibits PI3K/AKT pathway activity. Conversely, overexpression of UBXN1 increases cellular resistance to sorafenib, activates the PI3K/AKT pathway, and induces macrophage polarization toward the M2 phenotype. In vivo experiments further demonstrate that UBXN1 knockdown enhances the sensitivity of liver cancer cells to sorafenib and significantly reduces PI3K/AKT pathway activity. Our findings suggest that targeting UBXN1 may represent a promising therapeutic strategy to overcome sorafenib resistance in liver cancer. - Source: PubMed
Publication date: 2026/01/27
Li ManqiXie YuxinWei JinruiWu Lichuan - Porcine reproductive and respiratory syndrome virus (PRRSV) nonstructural protein 9 (NSP9), the viral RNA-dependent RNA polymerase (RdRp), is essential for viral replication but its comprehensive host interactome remains uncharacterized. This study employed co-immunoprecipitation coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS) to systematically identify NSP9-associated host proteins. We identified 222 high-confidence host interactors, with Gene Ontology and KEGG pathway analyses revealing significant enrichment in RNA/DNA-binding proteins, ubiquitin-proteasome pathways, metabolic regulators (amino acid/lipid biosynthesis), endoplasmic reticulum processing, and cell cycle components. Protein-protein interaction network analysis further delineated six functional modules involved in RNA processing, vesicular transport, and innate immunity. Crucially, validation studies confirmed direct binding between NSP9 and key candidates (CAPZ1, PSMA3, CDK1, USP48). Functional assessment demonstrated that CDK1 overexpression significantly inhibited PRRSV replication, implicating CDK1 as a host restriction factor. These findings collectively unveil the multifaceted role of NSP9 in subverting host machinery while identifying novel host defense mechanisms and potential targets for antiviral development against PRRSV. - Source: PubMed
Publication date: 2025/12/05
Wen WeiLiu YuhangWang WenqiangZhu ZhenbangLi Xiangdong - Clear cell renal cell carcinoma (ccRCC) is characterized by profound lipid metabolic dysregulation, yet the mechanisms linking peritumoral adipose tissue (PAT)-derived lipid metabolites to tumor aggressiveness remain poorly defined. Here, we identified lysophosphatidylethanolamine 18:1 (LPE18:1), a lipid metabolite enriched in PAT and the arterial blood of ccRCC patients, as a critical driver of tumor growth and lipid deposition. Through multiomics analyses and functional studies, we demonstrated that LPE18:1 upregulates F-actin-capping protein subunit alpha-1 (CAPZA1), which recruits ubiquitin-specific peptidase 48 (USP48) to stabilize the NAD-dependent protein deacetylase sirtuin-6 (SIRT6) by inhibiting its proteasomal degradation. Increased SIRT6 epigenetically promotes acetyl-CoA acetyltransferase 2 (ACAT2) expression, redirecting lipid metabolism toward free cholesterol accumulation-a hallmark of ccRCC aggressiveness. Clinically, CAPZA1 and SIRT6 levels correlate with advanced tumor stage and poor prognosis in ccRCC cohorts. Genetic or pharmacological inhibition of the CAPZA1/SIRT6 axis can reverse LPE18:1-induced lipid deposition and tumor progression in xenograft models. Notably, targeting this axis with the SIRT6 inhibitor OSS-128167 combined with CAPZA1 depletion significantly suppresses ccRCC cell growth. Our study reveals a PAT-derived lipid metabolite-fuelled signaling cascade that reprograms lipid metabolism in ccRCC, identifying CAPZA1/USP48/SIRT6 as actionable therapeutic targets for metabolic malignancies. - Source: PubMed
Publication date: 2025/12/08
Yue NanxiZhao HongyeZhang YongGu JunfeiQi JinchunWen JinkunWang WeiLv MingmingSun HaoChen JinsuoYang ChenxiaoQu ChangbaoChen XiaonanYang Zhan - Colorectal cancer (CRC) is the third malignant tumor in incidence rate and the second leading cause of cancer death worldwide. The progression of CRC is associated with both autophagy and ubiquitin-specific proteases (USPs). While USPs have been shown to regulate autophagy, their specific involvement in CRC autophagy remains largely unexplored. Herein, through the analysis of autophagy-related protein expression levels and proteomics, we found that high expression of USP48 was closely related to the inhibition of autophagy in CRC. And further analysis of CRC tissues showed that USP48 served as an independent risk factor for CRC patient prognosis. In vitro, we observed that USP48 significantly enhanced the proliferative, migration and invasion capacities of CRC cells. In vivo experiments showed that USP48 knockdown significantly inhibited the growth of subcutaneous tumors in nude mice, and the deletion of USP48 in intestinal epithelial cells reduced the number of intestinal tumors and mortality rate of mice. Mechanistically, USP48 was found to interact with the autophagy substrate protein sequestosome 1 (SQSTM1) and induce its deubiquitination at K420. This process inhibited autophagy, consequently maintaining the protein stability of SQSTM1. Rescue experiments demonstrated that SQSTM1 was the key target for USP48 to inhibit autophagy and promote CRC progression. Based on these findings, we constructed a tetrahedral DNA nanomaterial loaded with USP48 small interfering RNA (siRNA), which could effectively inhibited the progression of CRC in vivo while exhibiting excellent biocompatibility. In summary, our findings highlighted the role of USP48 in promoting CRC progression via the stabilization of SQSTM1, which leads to the suppression of autophagy. Thus, USP48 may be a potential therapeutic target for CRC. - Source: PubMed
Publication date: 2025/11/26
Li JuanLiu AijingDuan WeiliLi YanruKong XueWang TiantianNiu DunLiu ShaojunZhang PengWang ChuanxinLi PeilongDu Lutao