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
- 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 - Microglia dynamically support brain health through the induction of specialized activation states in response to injury or disease. Activation of the interferon-responsive microglia (IRM) state has been identified across neurodevelopmental windows, age-related cognitive decline, and neurodegenerative diseases. Functionally, IRM have been linked to synaptic pruning, dead cell removal, and neuroinflammation, making this state critical to brain homeostasis. While the functional importance of this state is becoming increasingly clear, our understanding of the regulatory networks that govern IRM induction remain incomplete. To systematically identify genetic regulators of the IRM state, we conducted a genome-wide CRISPR interference screen in human iPSC-derived microglia using IFIT1 as a representative IRM marker. We identified 772 genes that modulate IRM, including canonical type I interferon signaling genes () and newly described regulators. We uncovered a non-canonical role for the CCR4-NOT transcription complex subunit 10, , in IRM activation. This work provides a comprehensive resource that can be applied to dissect the functions of interferon-responsive microglia and highlights both established and novel targets for modulating microglial interferon signaling in health and disease. - Source: PubMed
Publication date: 2026/09/02
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