Ask about this productRelated genes to: USP18 antibody
- Gene:
- USP18 NIH gene
- Name:
- ubiquitin specific peptidase 18
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 22q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-16
- Date modifiied:
- 2018-02-28
Related products to: USP18 antibody
Related articles to: USP18 antibody
- Osteoporosis (OP) is a systemic metabolic disease associated with inflammation and apoptosis of osteoblasts. Ubiquitin-specific protease 18 (USP18) has been shown to participate in the progression of bone metabolic disorders; however, its role in osteoblast injury remains unclear. A rat OP model was established via bilateral ovariectomy (OVX). Pathological changes were observed using H&E and Masson staining, and Western blotting was used to detect the expression of related proteins. In vitro, an inflammatory injury model was constructed by inducing MC3T3-E1 mouse osteoblasts with 1 µg/mL LPS. CCK-8, EdU, flow cytometry, and Co-IP were utilized to validate the role of USP18 in osteoblast injury. OVX-treated rat femoral tissue samples exhibited severe inflammatory cell infiltration and bone damage. USP18 expression was significantly downregulated in OP rats and in LPS-stimulated osteoblasts. Overexpression of USP18 significantly increased cell viability and proliferation; upregulated the expression of osteogenesis-related protein markers (Runx2, ALP, and OCN); and reduced the levels of inflammatory factors (TNF-α and IL-6) and apoptotic proteins (Bax and cleaved caspase-3), thereby ameliorating LPS-induced osteoblast injury. Mechanistic studies revealed that USP18 binds to TAK1, removes K63-linked ubiquitination modifications on TAK1, and inhibits the activation of the p38/JNK-MAPK pathway. Notably, the MAPK activator anisomycin or TAK1 overexpression weakened the protective effects of USP18 on osteoblasts. USP18 inhibits MAPK pathway activation by deubiquitinating TAK1 and alleviates LPS-induced inflammation and apoptosis in osteoblasts. Furthermore, USP18 overexpression mitigates OP progression. - Source: PubMed
Publication date: 2026/09/25
Chen GuopingLiang JinlongCui YiWei JiahengXu Yongqing - Microglial ferroptosis is a key risk factor promoting neuroinflammation after ischemic brain injury (IBI). Although Compound 21 (C21) has neuroprotective and anti-inflammatory properties, its role in modulating microglial ferroptosis in IBI remains unexplored. - Source: PubMed
Publication date: 2026/09/25
Wu YijiuZhou XinqianHuo XufangHuang YouSheng DuanyangZeng Qingfan - This study aimed to investigate the testicular injury induced by PM2.5 and the associated enhancement of NLRP3/caspase-1/GSDMD-related pyroptotic signaling in rats by integrating animal experiments with public transcriptomic analysis. - Source: PubMed
Publication date: 2026/09/15
Luo YiWang CaoTian MengxiLang GuangyouLi KaixinZhang ZhongyanChu YuXiao QingHong Ma - Diabetes accelerates cardiac aging, but the molecular mechanisms that link metabolic stress to myocardial senescence remain insufficiently defined. This study investigated factors driving diabetes-associated cardiac aging with a focus on the role of USP18. Type 2 diabetes mellitus (T2DM) was induced in mice using a high-fat diet combined with streptozotocin. Cardiac structure, function, and molecular alterations were evaluated by echocardiography, histology, RNA sequencing, western blotting, qPCR, and immunofluorescence. H9C2 cardiomyocytes cultured under high-glucose conditions were used for in vitro validation. Diabetic mice exhibited diastolic dysfunction, myocardial hypertrophy, and fibrosis, accompanied by increased p53 and p21 expression. RNA-seq and protein analyses consistently identified USP18 as significantly upregulated in diabetic hearts. Elevated USP18 was associated with activation of the cGAS-STING pathway, increased TBK1 phosphorylation, and enhanced IL-6 and IL-1β production. High-glucose-treated cardiomyocytes similarly showed USP18 induction, stabilization of cGAS-STING signaling, and enhanced senescence-related responses. USP18 contributes to cardiac aging in diabetes by promoting cGAS-STING activation and inflammatory senescence. Targeting USP18 may represent a potential strategy to alleviate myocardial aging under diabetic conditions. - Source: PubMed
Deng XunxiYin ZhiyiTai ShiJiang HejunZhou YuyingWang YongjunFu Liyao - Varicocele (VC) represents a primary etiology of male infertility, yet the epigenetic landscapes and molecular triggers driving VC-associated spermatogenic failure remain largely enigmatic. Herein, it is demonstrated that Sertoli cell ferroptosis is a critical pathological feature of VC, and its pharmacological inhibition effectively rescues VC-induced reproductive impairment . Through small RNA sequencing of clinical testicular tissues, piRNA-46403 is identified as a significantly upregulated mediator in VC patients with asthenospermia. Functionally, piRNA-46403 is shown to orchestrate Sertoli cell ferroptosis, whereas its silencing attenuates spermatogonial apoptosis and restores spermatogenic function. Mechanistically, piRNA-46403 acts as a molecular decoy that binds to the RNA-binding protein YBX1. This interaction disrupts the binding of YBX1 to m5C-modified USP18 mRNA, thereby reducing USP18 mRNA stability and triggering ferroptosis. These findings elucidate a novel piRNA-46403/YBX1/m5C-modified USP18 regulatory axis in the male reproductive system and position piRNA-46403 as a promising therapeutic target for mitigating VC-mediated infertility. - Source: PubMed
Publication date: 2026/08/12
Fang XiaoSong LiLiu DongXin ZhixiangPang WenjuanTong QiangHuang JingWang AnbangYin LeiHuang HejingJiang AiminRen Shancheng