Ask about this productRelated genes to: Rnf183 antibody
- 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 antibody
Related articles to: Rnf183 antibody
- 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 - Regulated cell death (RCD), a genetically controlled process mediated by specialized molecular pathways (commonly termed programmed cell death), plays pivotal roles in diverse pathophysiological processes. However, the landscape and functional implications of RCD subtypes in chronic rhinosinusitis with nasal polyps (CRSwNP) remain poorly characterized. This study aimed to systematically investigate the involvement of RCD mechanisms in the pathogenesis and progression of CRSwNP. - Source: PubMed
Publication date: 2025/03/29
Li Hong-XiaFei JingXu WeiPeng YiYan Pi-JunXu YongQin GangTeng Fang-Yuan - Diabetic kidney disease (DKD) is a prevalent complication associated with diabetes in which podocyte dysfunction significantly contributes to the development and progression of the condition. Ring finger protein 183 (RNF183) is an ER-localized, transmembrane ring finger protein with classical E3 ligase activity. However, whether RNF183 is involved in glomerular podocyte dysfunction, which is the mechanism of action of DKD, is still poorly understood. In this study, we first demonstrated that RNF183 expression in glomerular podocytes of patients with DKD decreased as the disease progressed. Additionally, our transcriptome sequencing analysis of kidney tissues from diabetic mice revealed a significant reduction in RNF183 expression within the kidney cortex. Similarly, the expression of RNF183 was significantly reduced both in the kidneys of diabetic mice and in human podocytes exposed to high glucose conditions. The downregulation of RNF183 resulted in a suppression of autophagic activity, an increase in apoptotic cell death, and reduced expression of cellular markers in HPC cells. We found that RNF183 was modified via N6-methyladenosine (m6A) RNA methylation. Meanwhile, treatment with meclofenamic acid 2 (MA2), an m6A demethylase inhibitor, resulted in the upregulation of RNF183 expression in HPC cells cultured in high glucose conditions. Furthermore, high glucose treatment decreased the transcription and protein levels in both the m6A writer methyltransferaselike3 (METTL3) and the m6A reader insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2). IGF2BP2 assisted with METTL3, which is jointly involved in the transcription of RNF183. Furthermore, we confirmed that RNF183 directly ubiquitinates M2 pyruvate kinase (PKM2) through co-immunoprecipitation (Co-IP) and liquid chromatography-mass spectrometry (LC-MS) experiments. The level of PKM2 ubiquitination was increased following RNF183 overexpression, leading to enhanced PKM2 protein degradation and subsequently alleviating high glucose-induced podocyte damage. The results of this study indicated that RNF183 was regulated via m6A methylation modification and that RNF183 expression was reduced in HPC cells treated with high glucose, which resulted in decreased PKM2 ubiquitination levels and subsequently aggravated podocyte injury. The findings suggest that RNF183 may serve as a potential therapeutic target for diabetic kidney injury, offering new insights into its role in the progression of DKD. - Source: PubMed
Publication date: 2025/03/01
Guo DongweiPang YingxueWang WenjieFeng YueyingWang LuxuanSun YuanyuanHao JunLi FanZhao Song