Ask about this productRelated genes to: RNF182 antibody
- Gene:
- RNF182 NIH gene
- Name:
- ring finger protein 182
- Previous symbol:
- -
- Synonyms:
- MGC33993
- Chromosome:
- 6p23
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-26
- Date modifiied:
- 2019-03-19
Related products to: RNF182 antibody
Related articles to: RNF182 antibody
- : Glioblastoma (GBM) is the most common and aggressive brain tumor in adults. Changes in the ubiquitination system in GBM cells can promote uncontrolled tumor growth and reduce the effectiveness of treatments. However, the exact targets and regulatory elements of the ubiquitin-proteasome system involved in GBM are still not well understood. : All data were obtained by using in silico analysis, immunohistochemistry, Western blot, RT-qPCR, gene silencing and proliferation assay. : Computational and protein analyses show that aggressive gliomas have higher expression of the RING ligase RNF182, with significantly greater levels in glioblastoma (GBM) than in low-grade gliomas. Elevated RNF182 is strongly associated with GBM growth. Experiments using siRNA to inhibit RNF182 in the human glioblastoma cell line U87MG significantly reduced cell proliferation, suggesting that RNF182 promotes tumor growth and may be a potential therapeutic target. : These findings create a connection between the ubiquitin-proteasome system and the unchecked growth observed in GBM, identifying RNF182 as a new marker associated with GBM proliferation and an additional target for GBM treatment. - Source: PubMed
Publication date: 2026/04/11
Russo VeronicaRusso MiriamOliva Maria AntoniettaAlborghetti MarikaCaridi MatteoGiangaspero FeliceArcella Antonietta - Research shows that patients with viral pneumonia complicated by diabetes have a worse prognosis and higher mortality. Our study aimed to assess the effect of diabetes on respiratory tract microbes and the transcriptome in patients with viral pneumonia. We included 76 subjects from China-Japan Friendship Hospital, including 16 healthy people, 17 patients with viral pneumonia and diabetes (VD), and 43 patients with viral pneumonia without diabetes (VP). We collected their sputum samples for both metagenomic and 16S rRNA sequencing and collected blood samples for RNA sequencing. In transcriptome analysis, the VD group downregulated the expression of PTCH1 and upregulated the expression of ANK1, RBM38, BPGM, CRYM, TAL1, and HBD. The differential pathways are mainly reflected in the formation, development, and maintenance of red blood cells, the activity of immunoglobulins, and the membrane transport and transportation of substances. There is a significant difference in microbial diversity between the two groups. Both analysis methods demonstrate a significant increase in the abundance of , and in the VP group. The host genes AGAP1, RNF182, and ANKRD9 are particularly closely associated with microorganisms. Our results suggest that diabetes may inhibit the expression of genes related to immune regulation, energy metabolism, and oxygen utilization in patients with viral pneumonia. Meanwhile, we predict that VD may be associated with a decrease in microbial diversity and a decline in microbial functions in cellular processes, environmental adaptation, metabolism, and genetic activity. These abnormalities can worsen the course of viral pneumonia and affect the prognosis of patients. - Source: PubMed
Publication date: 2026/04/06
Huang ChangruiFeng QinqiYu BangZou HaoCai YashiLiu JianLi DeminZhang HongchunZou Xiaohui - We aimed to identify the strongest individual gene-respiratory interactions for rheumatoid arthritis (RA) risk. - Source: PubMed
Publication date: 2026/01/30
Kronzer Vanessa LBrooks Rebecca TShurtz Anne KWang XiaosongAtkinson Elizabeth JDavis John MSparks Jeffrey ACerhan James RJoerns Elena KVassallo RobertCrowson Cynthia S - Intervertebral disc degeneration (IVDD) is a prevalent disorder associated with chronic inflammation, significantly affecting spinal health and general quality of life. This study examines the anti-inflammatory properties of Friedelin (FD) and its impact on the NF-κB signalling pathway in relation to IVDD. In vivo experiments utilising cervical intervertebral disc tissue from mice exhibiting cervical spine instability and in vitro assays with nucleus pulposus (NP) cells revealed that FD treatment significantly diminished NP degeneration and inflammatory cytokine production, concurrently inhibiting NF-κB activation. FD triggered autophagic clearance of p65, reducing inflammatory cytokine output. This effect was mediated by selective inhibition of p65 phosphorylation, independent of IKK activity, highlighting its targeted action on NF-κB signalling. Moreover, FD enhanced the association between p65 and the E3 ubiquitin ligase RNF182, facilitating p65 degradation via autophagy. The findings indicate that FD mitigates IVDD by diminishing NP degradation and inflammation while also presenting a potential therapeutic strategy that targets the NF-κB signalling pathway through autophagic processes. - Source: PubMed
Tu KewuLiao DongtengChen ZhaomouWang ZhenyuZhao KunZhong HongyuWu ShiminZhu HuiyinXu JinmingZhou BeidiDai XianghengWu Qiang - Renal fibrosis is a major driver of chronic kidney disease (CKD) progression, yet targeted therapies remain limited due to incomplete understanding of key molecular mechanisms. While IL-1-mediated inflammation and mitochondrial dysfunction are recognized contributors, the precise links between IL-1 signaling, fibrosis, and mitochondrial homeostasis are unclear. Here, we investigated the therapeutic effects of recombinant human IL-1 receptor antagonist (rhIL-1Ra) in both acute (UUO) and chronic (5/6Nx) mouse models of kidney injury, as well as in vitro TGF-β1-stimulated kidney cells. rhIL-1Ra significantly attenuated renal fibrosis, inflammation, and functional impairment in vivo. Mechanistically, rhIL-1Ra suppressed TGF-β1-induced expression of the E3 ubiquitin ligase RNF182, which we show mediates MFN2 ubiquitination and degradation, leading to mitochondrial dysfunction. Inhibition of RNF182 by rhIL-1Ra stabilized MFN2, preserved mitochondrial respiration and ATP production, and reduced oxidative stress. Rescue experiments confirmed the centrality of the RNF182-MFN2 axis in fibrotic and mitochondrial injury. Our findings reveal a novel IL-1R/RNF182/MFN2 pathway linking inflammation to mitochondrial and fibrotic pathology, supporting RNF182 as a promising target and rhIL-1Ra as a potential therapy for CKD. - Source: PubMed
Publication date: 2025/12/29
Yang BoShao QingWang WeiLi MaotingZeng FanzhouFu XueziLiu JunXue ChengLiu Nanmei