Ask about this productRelated genes to: Rnf183 Blocking Peptide
- Gene:
- RNF183 NIH gene
- Name:
- ring finger protein 183
- Previous symbol:
- -
- Synonyms:
- MGC4734
- Chromosome:
- 9q32
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-28
- Date modifiied:
- 2019-03-19
Related products to: Rnf183 Blocking Peptide
Related articles to: Rnf183 Blocking Peptide
- Hypertensive retinopathy is a microvascular complication caused by systemic hypertension and can lead to severe visual impairment. At present, the molecular mechanisms of this disease remain incompletely understood, particularly the global expression profiles and regulatory networks of non-coding RNA (ncRNA). This study aims to comprehensively analyze the genome-wide differential expression profiles of messenger RNA (mRNA), microRNA (miRNA), long non-coding RNA (lncRNA), and circular RNA (circRNA) in retinal tissues from a spontaneously hypertensive rat (SHR) model of hypertensive retinopathy, and to observe transcriptomic changes after treatment with the calcium channel blocker lacidipine, thereby revealing their potential roles in disease pathogenesis and identifying possible therapeutic targets. - Source: PubMed
Shi WenXiao ShiyuanBu BingHuang TianxinJiang YiranJiang Wenmin - Macrophage polarization affects the progression of lung cancer. This study aimed to explore the potential mechanism whereby M2 macrophages accelerate the progression of lung cancer. - Source: PubMed
Publication date: 2026/07/08
Xu LuLu Chenlin - RING-finger protein 183 (RNF183) is a ubiquitin ligase specifically expressed in the kidney and especially in collecting ducts that are constantly exposed to hypertonic stress. The expression of RNF183 in the colon is low but is upregulated in patients with inflammatory bowel disease (IBD) and patients with colorectal cancer. However, the function and relationship of RNF183 with these diseases remain unclear. Here, we identify the Na-K-2Cl co-transporter NKCC1 as a substrate of RNF183. RNF183 promotes K63-linked ubiquitination of NKCC1, leading to its lysosomal degradation, which is enhanced under hypertonic conditions. Dysregulation of RNF183 expression increases hypertonic-induced cell death in Rnf183-knockout mIMCD-3 cells and RNF183-overexpressing Caco-2 cells, accompanied by an increase in cleaved caspase-3. Under isotonic and hypertonic conditions, intracellular Na homeostasis is disrupted in these cells. Notably, RNF183 expression exerts opposing effects in mIMCD-3 cells, which endogenously express RNF183, and in Caco-2 cells, which do not. Thus, RNF183, which targets multiple ion transporters, including NKCC1 identified in this study, may play an important role in the adaptation to hypertonic conditions in the kidney, whereas aberrant expression of RNF183 could cause the development of diseases such as IBD and colorectal cancer. - Source: PubMed
Publication date: 2026/04/06
Okamoto TakumiHigashi YukiTakemoto MasaakiMatsuhisa KojiSato ShinyaSaito AtsushiOmura IsseiKamikawa YasunaoImaizumi KazunoriKaneko Masayuki - The dysregulation of genes related to lipid metabolism and lysosomal function has been reported to significantly contribute to tumor progression. In this study, we systematically explored the roles played by lipid metabolism and lysosomes in uterine corpus endometrial carcinoma (UCEC), aiming to identify potential biomarkers for predicting prognosis and immune checkpoint therapy efficacy. - Source: PubMed
Publication date: 2025/09/08
Zhu YuanyuanYang PushengZhang Shu - Hyperglycemia is a recognized risk factor for bladder cancer (BC). Enfortumab vedotin (EV), the first NECTIN4-targeting antibody-drug conjugate, demonstrates promising clinical efficacy in patients with advanced BC. In this study, we show that EV treatment is less effective in BC patients with diabetes than in those with normoglycemia. The subsequent in vitro and in vivo experiments indicate that high glucose decreases the sensitivity of BC cells to EV. Mechanistically, lactate overproduction associated with high glucose promotes AARS1-mediated YTHDC1 lactylation and enhances RNF183-mediated YTHDC1 ubiquitination. Downregulated YTHDC1 reduces JUND mRNA stability in an mA-dependent manner, subsequently decreasing NECTIN4 expression and EV responsiveness. Our study identifies a high-glucose-associated lactate-AARS1-YTHDC1-JUND-NECTIN4 axis that affects EV sensitivity in BC. Targeting this axis with JUND activators or β-alanine may offer therapeutic strategies to enhance the sensitivity of BC cells to EV. - Source: PubMed
Publication date: 2025/04/10
Xing ZhuoYang TiejunLi XuruiXu HaozheHong YulongShao ShuaiLi TaoYe LiefuLi YuanJin XinWei Yongbao