Ask about this productRelated genes to: RNF182 Blocking Peptide
- 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 Blocking Peptide
Related articles to: RNF182 Blocking Peptide
- 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 - Innate immunity is the first line of antiviral or antimicrobial defence for the host. A cytoplasmic viral RNA sensor, which is known as retinoic acid-inducible gene 1 (RIG-I), makes a vital impact on the production of type I interferons (IFN) and eliminating RNA virus. This study indicated that E3 ubiquitin ligase RING finger protein 182 (RNF182) inhibited the antiviral activity of type I IFN in grass carp reovirus (GCRV)-infected cells by directly interplaying with RIG-I. The CiE3RNF182 cDNA encode a polypeptide of 158 amino acids. Cellular distribution analysis results suggested that cytoplasm was the main site of CiE3RNF182 location. Real-time quantitative PCR showed universal expression of CiE3RNF182 in all investigated tissues, with extremely high expression in liver. During virus infection, the CiE3RNF182 associates with the CiRIG-I and then induces the Lys-33-linked ubiquitin to the Lys33 residues of CiRIG-I to trigger its degradation, causing the inhibition of CiRIG-I downstream signalling. Furthermore, we obtained CRISPR/Cas9-mediated generation of E3RNF182-null rare minnows, finding that E3RNF182 deletion facilitates the survival ratio of GCRV-infected rare minnows. Additionally, the E3RNF182 rare minnows exhibited significantly lower relative copy number of GCRV compared to the wild-type group. In summary, our findings demonstrate the function of E3 ligase in controlling the anti-GCRV innate immunity through RIG-I in fish. - Source: PubMed
Publication date: 2025/03/04
Lin YushengFeng HaohaoWang YuxuanLiu ShuaiHu PengchengWang JingCao Hong