Ask about this productRelated genes to: COMMD8 Blocking Peptide
- Gene:
- COMMD8 NIH gene
- Name:
- COMM domain containing 8
- Previous symbol:
- -
- Synonyms:
- FLJ20502
- Chromosome:
- 4p12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-13
- Date modifiied:
- 2014-11-19
Related products to: COMMD8 Blocking Peptide
Related articles to: COMMD8 Blocking Peptide
- The role and mechanistic action of MNX1-AS1 in non-small cell lung cancer (NSCLC) remain unclear. This study aimed to investigate the function of MNX1-AS1 in the progression of NSCLC. A total of 40 paired tumor and adjacent lung tissue samples from patients with NSCLC were collected to investigate the expression of MNX1-AS1. H1299 and HCC827 cells were transfected with sh-MNX1-AS1, shRNA-NC, miR-218-5p mimic, mimic-NC, pcDNA3.1-COMMD8, or empty vector (pcDNA3.1). The expression of MNX1-AS1, miR-218-5p, and COMMD8 was detected using quantitative real-time PCR (qRT-PCR). Cell proliferation was evaluated using CCK-8 assays, while cell migration and invasion were evaluated using Transwell assays. Dual-luciferase reporter and RNA pull-down assays were performed to validate the targeting interactions between MNX1-AS1 and miR-218-5p, as well as between COMMD8 and miR-218-5p. In vivo, a nude mouse model was established: tumor volume and weight were measured after four weeks. Gene expression in tumor tissue was quantified using qRT-PCR, and Ki-67 expression was evaluated using immunohistochemistry. MNX1-AS1 expression was significantly upregulated in NSCLC tissues (P < 0.05) and was correlated with poor prognosis in NSCLC patients. MNX1-AS1 knockdown markedly suppressed the viability, migration, and invasion of H1299 and HCC827 cells (P < 0.05). Mechanistically, MNX1-AS1 acted as a molecular sponge for miR-218-5p, thereby relieving miR-218-5p-mediated repression of its direct target COMMD8 (P < 0.05). Functional rescue experiments revealed that miR-218-5p silencing or COMMD8 overexpression partially reversed the inhibitory effects of MNX1-AS1 knockdown on the cell viability, migration, and invasion of H1299 and HCC827 cells. In vivo, sh-MNX1-AS1 significantly reduced tumor volume and weight (P < 0.05). Moreover, the expression of MNX1-AS1, COMMD8, and Ki-67 were downregulated, while the expression of miR-218-5p was upregulated in sh-MNX1-AS1 tumor tissues (P < 0.05). MNX1-AS1 promotes the progression of NSCLC by modulating the miR-218-5p/COMMD8 axis. - Source: PubMed
Publication date: 2026/07/29
Liu Gao-FengZhou LiZhao Yu-BoTang Jia-HongLi Qing-YuanDing Xiao-YongZhang Xiao-ZhenCui Su-JuanZhang YongSun Zhen-Wei - Rheumatoid arthritis (RA) and major depressive disorder (MDD) exhibit significant comorbidity, with shared pathological mechanisms such as inflammation and abnormal lipid metabolism. However, the specific molecular features and functional pathways linking the two diseases remain unclear. - Source: PubMed
Publication date: 2026/05/26
Liu JiaruXiang CuitianZhou QiruiDing ZhenzhuWang JingrongLi Arong - The COMMD (copper metabolism MURR1 domain-containing) protein family, characterized by a conserved COMM domain, plays crucial roles in metal ion transport and NF-κB signaling regulation in vertebrates. However, its functional roles in invertebrates, particularly crustaceans, remain poorly understood. This study aimed to identify and characterize COMMD family genes in red swamp crayfish (Procambarus clarkii) and to investigate their involvement in immune responses under environmental stress. - Source: PubMed
Publication date: 2025/11/13
Zhang XinCai XiuhongYue ShiruiChen ZhangxuanSun YulongWang Shunchang - The epigenetic modifier N6-methyladenosine (m6A), recognized as the most prevalent internal modification in messenger RNA (mRNA), has recently emerged as a pivotal player in immune regulation. Its dysregulation has been implicated in the pathogenesis of various autoimmune conditions. However, the implications of m6A modification within the immune microenvironment of Sjögren's syndrome (SS), a chronic autoimmune disorder characterized by exocrine gland dysfunction, remain unexplored. Herein, we leverage an integrative analysis combining public database resources and novel sequencing data to investigate the expression profiles of m6A regulatory genes in SS. Our cohort comprised 220 patients diagnosed with SS and 62 healthy individuals, enabling a comprehensive evaluation of peripheral blood at the transcriptomic level. We report a significant association between SS and altered expression of key m6A regulators, with these changes closely tied to the activation of CD4 T cells. Employing a random forest (RF) algorithm, we identified crucial genes contributing to the disease phenotype, which facilitated the development of a robust diagnostic model via multivariate logistic regression analysis. Further, unsupervised clustering revealed two distinct m6A modification patterns, which were significantly associated with variations in immunocyte infiltration, immune response activity, and biological function enrichment in SS. Subsequently, we proceeded with a screening process aimed at identifying genes that were differentially expressed (DEGs) between the two groups distinguished by m6A modification. Leveraging these DEGs, we employed weight gene co-expression network analysis (WGCNA) to uncover sets of genes that exhibited strong co-variance and hub genes that were closely linked to m6A modification. Through rigorous analysis, we identified three critical m6A regulators - , , and - alongside two m6A-related hub genes, and . These elements collectively underscore a complex but discernible pattern of m6A modification that appears to be integrally linked with SS's pathogenesis. Our findings not only illuminate the significant correlation between m6A modification and the immune microenvironment in SS but also lay the groundwork for a deeper understanding of m6A regulatory mechanisms. More importantly, the identification of these key regulators and hub genes opens new avenues for the diagnosis and treatment of SS, presenting potential targets for therapeutic intervention. - Source: PubMed
Publication date: 2024/03/29
Yin JunhaoFu JiayaoXu JiabaoChen ChangyuZhu HanyiWang BaoliYu ChuangqiYang XiujuanCai RuiyuLi MengyangJi KaihanWu WanningZhao YijieZheng ZhanglongPu YipingZheng Lingyan - Celastrol, a bioactive molecule extracted from the plant, has been shown to exhibit anti-inflammatory properties. However, its mechanism of action has not been fully elucidated. Here, we show that celastrol suppresses humoral immune responses and autoimmunity by disabling a protein complex consisting of copper metabolism MURR1 domain-containing (COMMD) 3 and COMMD8 (COMMD3/8 complex), a signaling adaptor for chemoattractant receptors. Having demonstrated the involvement of the COMMD3/8 complex in a mouse model of rheumatoid arthritis, we identified celastrol as a compound that covalently bound to and dissociated the COMMD3/8 complex. Celastrol inhibited B cell migration, reduced antibody responses, and blocked arthritis progression, recapitulating deficiency of the COMMD3/8 complex. These effects of celastrol were abolished in mice expressing a celastrol-resistant mutant of the COMMD3/8 complex. These findings establish that celastrol exerts immunosuppressive activity by targeting the COMMD3/8 complex. Our study suggests that the COMMD3/8 complex is a potentially druggable target in autoimmune diseases and points to celastrol as a lead pharmacologic candidate in this capacity. - Source: PubMed
Publication date: 2023/03/31
Shirai TaiichiroNakai AkikoAndo EmikoFujimoto JunLeach SarahArimori TakaoHigo Daisukevan Eerden Floris JTulyeu JanyerkyeLiu Yu-ChenOkuzaki DaisukeMurayama Masanori AMiyata HaruhikoNunomura KazutoLin BangzhongTani AkiyoshiKumanogoh AtsushiIkawa MasahitoWing James BStandley Daron MTakagi JunichiSuzuki Kazuhiro