USP11 Antibody
- Known as:
- USP11 Antibody
- Catalog number:
- abx008540
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- USP11 Antibody
Related genes to: USP11 Antibody
- Gene:
- USP11 NIH gene
- Name:
- ubiquitin specific peptidase 11
- Previous symbol:
- -
- Synonyms:
- UHX1
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-01
- Date modifiied:
- 2016-10-05
Related products to: USP11 Antibody
Related articles to: USP11 Antibody
- Liver fibrosis represents a central pathological process in chronic liver diseases and poses a severe threat to human health. Cuproptosis, a copper ion-dependent form of regulated cell death, offers a potential therapeutic strategy for liver fibrosis. This study demonstrated that dihydroartemisinin (DHA) transiently upregulates SLC31A1, thereby promoting copper influx. Under copper overload, SLC31A1 undergoes ubiquitin-mediated degradation, while DHA targets RAB1B to activate RAB10-dependent vesicular endocytosis as a compensatory mechanism for sustained copper accumulation. This endocytic process alters cellular biomechanical properties and strengthens RAB1B-VDAC1 interaction to promote mitochondrial copper uptake. Following cuproptosis, iron-sulfur cluster proteins undergo degradation, leading to massive iron release and subsequent ferroptosis, establishing a cascading dual cell death mechanism. Mechanistically, RAB1B regulates KAT2A-mediated succinylation of USP11, thereby inhibiting USP11's deubiquitinating activity and accelerating SLC31A1 degradation. For applications, we engineered biomimetic nanoliposomes coated with HSC membranes and surface-functionalized with CD47, FNIII10, and ApoE. This system integrates immune evasion, hepatic accumulation, and HSC-specific recognition capabilities, demonstrating remarkable targeting efficacy and mechanistic consistency in primary HSCs and rodent models. These findings reveal that DHA enhances copper-laden vesicular endocytosis by targeting RAB1B, thereby triggering cuproptosis and ferroptosis, and provide novel molecular targeting strategies for liver fibrosis therapy. - Source: PubMed
Publication date: 2026/07/22
Qiu XinranTian HaoyuanSun ShujiangQiu NingyuXu BiaoWang JunruiGao YuanyuanBao ZhengyangHan XiangZeng JieLin YuxinZhang FengZheng ShizhongShao Jiangjuan - The orphan nuclear receptor NR2F1 has been shown to associate with a dormant tumor state in multiple tumor models. However, its dynamic regulation, particularly at the level of protein post-translational modification, remains largely unclear. In this study, we identify the deubiquitinase ubiquitin-specific peptidase 11 (USP11) as a potential regulator that controls the protein stability of NR2F1. USP11 directly interacts with NR2F1, and its overexpression increases NR2F1 protein level by suppressing NR2F1 protein turnover. Mechanistically, USP11 deubiquitinates NR2F1 at K70 and K369 to protect it from proteasomal degradation. Consistent with these findings, USP11 and NR2F1 expression levels are positively correlated across multiple tumor types. Notably, elevated expression of either USP11 or NR2F1 predicts a better prognosis in kidney renal clear cell carcinoma, indicating their potential clinical significance. Together, these findings reveal a post-translational regulatory mechanism of NR2F1 and suggest that targeting USP11 may provide a potential strategy for modulating tumor dormancy. - Source: PubMed
Publication date: 2026/08/31
Liu YeWu FaliangHuang JinpingCao MengdiWu YalanTang HuiTang Xiaolong - Chronic kidney disease (CKD) has emerged as a critical global health challenge, driven by its high prevalence and poor prognosis. Ubiquitin-specific protease 11 (USP11), a deubiquitinating enzyme, participates in DNA damage repair, cell-cycle regulation, and immune modulation, and has been shown to promote epithelial-mesenchymal transition in renal tubular epithelial cells (TECs) during CKD progression. However, whether USP11 also plays a critical role in the apoptosis of TECs remains to be elucidated. In this study, we demonstrate that USP11 deubiquitinates and stabilizes p53, thereby activating the p53-mediated canonical mitochondrial pathway of apoptosis in cultured human proximal TECs (HK-2). In uric acid (UA)-stimulated HK-2 cells, activated p53 subsequently increases mitochondrial outer membrane permeabilization (MOMP), leading to the release of cytochrome c from the mitochondria into the cytosol, which, in turn, activates caspase 9 and caspase 3, and ultimately promotes TEC apoptosis. Inhibition of USP11 with siRNA transfection or mitoxantrone (MTX), a small-molecule inhibitor of USP11, downregulates p53 expression and blocks cytochrome c release into the cytosol, thereby significantly reducing TEC apoptosis. In vivo, both conditional genetic knockout and pharmacological inhibition of USP11 effectively reduce apoptosis of tubular cells and ameliorate kidney injury in a mouse CKD model of hyperuricemic nephropathy (HN). In summary, our results underscore the pivotal role of USP11 in TEC apoptosis during CKD progression and suggest that targeting USP11 represents a potential therapeutic approach for CKD patients. - Source: PubMed
Publication date: 2026/08/18
Shi YingfengLi JinqingLiu Na - Myocardial Ischemia-Reperfusion Injury (MIRI) is a key pathological link in the treatment of myocardial infarction (MI), leading to further necrosis of cardiomyocytes and deterioration of cardiac function. The abnormal expression and function of voltage-dependent anion channel 1 (VDAC1) has been confirmed to be closely related to MIRI. This study aims to explore the effects and mechanisms of VDAC1 on MI development. - Source: PubMed
Publication date: 2026/08/26
Zheng WeiLiao XueyanCui WeiZhang MingZhao FengyingWang ZhiweiHu Qionghua - Pancreatic ductal adenocarcinoma (PDAC) is widely recognized as the most lethal malignancy of the digestive system. Its poor prognosis is largely attributed to a high degree of resistance to gemcitabine (GEM), highlighting the critical need to elucidate the underlying mechanisms of GEM resistance for effective therapeutic intervention. DLGAP5, a cell cycle-associated protein, has been implicated in PDAC progression; however, its potential role in regulating glycolysis and GEM resistance remains unclear. - Source: PubMed
Publication date: 2026/08/22
Tao PengxianChe YangZhang YanSu HeXie XiaodongCai Hui