ZNF883 Antibody - C-terminal region (ARP31644_P050)
- Known as:
- ZNF883 Antibody - C-terminal region (ARP31644_P050)
- Catalog number:
- arp31644_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF883 Antibody - C-terminal region (ARP31644_P050)
Related genes to: ZNF883 Antibody - C-terminal region (ARP31644_P050)
- Gene:
- ZNF883 NIH gene
- Name:
- zinc finger protein 883
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 9q32
- Locus Type:
- gene with protein product
- Date approved:
- 2010-03-17
- Date modifiied:
- 2014-11-19
Related products to: ZNF883 Antibody - C-terminal region (ARP31644_P050)
Related articles to: ZNF883 Antibody - C-terminal region (ARP31644_P050)
- This study focused on identifying potential key lncRNAs associated with gout under the mechanisms of copper death and iron death through ceRNA network analysis and Random Forest (RF) algorithm, which aimed to provide new insights into the molecular mechanisms of gout, and potential molecular targets for future therapeutic strategies of gout. Initially, we conducted an in-depth bioinformatics analysis of gout microarray chips to screen the key cuproptosis-related genes (CRGs) and key ferroptosis-related genes (FRGs). Using these data, we constructed a key ceRNA network for gout. Finally, key lncRNAs associated with gout were identified through the RF algorithm combined with ROC curves, and validated using the Comparative Toxicogenomics Database (CTD). We successfully identified NLRP3, LIPT1, and DBT as key CRGs associated with gout, and G6PD, PRKAA1, LIG3, PHF21A, KLF2, PGRMC1, JUN, PANX2, and AR as key FRGs associated with gout. The key ceRNA network identified four downregulated key lncRNAs (SEPSECS-AS1, LINC01054, REV3L-IT1, and ZNF883) along with three downregulated mRNAs (DBT, AR, and PRKAA1) based on the ceRNA theory. According to CTD validation inference scores and biological functions of target mRNAs, we identified a potential gout-associated lncRNA ZNF883/hsa-miR-539-5p/PRKAA1 regulatory axis. This study identified the key lncRNA ZNF883 in the context of copper death and iron death mechanisms related to gout for the first time through the application of ceRNA network analysis and the RF algorithm, thereby filling a research gap in this field and providing new insights into the molecular mechanisms of gout. We further found that lncRNA ZNF883 might function in gout patients by regulating PRKAA1, the mechanism of which was potentially related to uric acid reabsorption in the proximal renal tubules and inflammation regulation. The proposed lncRNA ZNF883/hsa-miR-539-5p/PRKAA1 regulatory axis might represent a potential RNA regulatory pathway for controlling the progression of gout disease. This discovery offered new molecular targets for the treatment of gout, and had significant implications for future therapeutic strategies in managing the gout. - Source: PubMed
Publication date: 2024/03/12
Shao Zi-ChenSun Wei-KangDeng Qin-QinCheng LingHuang XinHu Lie-KuiLi Hua-Nan - The goal of this study was to characterize the mechanisms of long noncoding RNA (lncRNA) ZNF883 regulating NOD-like receptor 3 (NLRP3) inflammasome activation in epilepsy (EP). Rat and cellular EP models were established using pilocarpine and magnesium-free extracellular fluid, respectively, to detect the differential expression of ZNF883, microRNA (miR)-138-5p, ubiquitin-specific peptidase 47 (USP47), and NLRP3. The pathology of the hippocampal neurons was examined by whole-cell patch clamping. The expression of ZNF883, miR-138-5p, and USP47 was modified in epileptic neurons, and the EP rats were injected with sh-ZNF883. Then, alterations in ZNF883, miR-138-5p, and USP47 levels were measured. The histopathology of the hippocampus was detected, along with the detection of IL-6, IL-1β, TNF-α, and NLRP3. Neuronal apoptosis in the rat and cellular EP models was determined. The relationship among ZNF883, miR-138-5p, and USP47 as well as the regulation of NLRP3 ubiquitination by USP47 was determined. ZNF883, USP47, and NLRP3 were increasingly expressed and miR-138-5p was downregulated in epileptic neurons and rats, concurrent with aggravated inflammation and apoptosis. ZNF883 overexpression in epileptic neurons elevated USP47 expression. ZNF883 targeted miR-138-5p and miR-138-5p negatively regulated USP47. In epileptic neurons, inhibiting miR-138-5p or overexpressing USP47 partially reversed the ZNF883 silencing-induced inhibition on NLRP3 inflammasome activation, neuronal apoptosis, and epileptiform activity. ZNF883 silencing in EP rats decreased USP47 and NLRP3, increased miR-138-5p, and inhibited inflammation and apoptosis. USP47 reversed the ubiquitination of NLRP3. ZNF883 inhibits NLRP3 ubiquitination and promotes EP through upregulating USP47 by sponging miR-138-5p. - Source: PubMed
Publication date: 2022/06/09
Gong LinaHan YaruChen RuYang PuZhang Chen - Epilepsy (EP) is a very dangerous neurological disease. MiR-181b was reported to play a regulatory role during the progression of EP. However, the mechanism by which miR-181b regulates the process of EP remains unclear. - Source: PubMed
Publication date: 2020/06/15
Gong LinaYang PuHu LingZhang Chen - Lung cancer is a leading cause of cancer mortality worldwide with dramatically increasing incidence in recent years. However, the mechanism underlying its progression remains unclear. The aim of this study was to identify the role of hypermethylated in cancer 1 (HIC1) in lung cancer development. Here we found that HIC1 expression was markedly decreased in lung cancer compared with the corresponding adjacent non-cancerous tissues. Meanwhile, overall survival (OS) of lung cancer patients was negatively related with HIC1 expression using TCGA and GEO datasets. Loss of HIC1 expression promoted cell proliferation and migration in vitro. Notable, HIC1 knock-out in Kras/sgHIC1 mice had remarkable effect on tumorigenesis compared with Kras/sgTd control mice. Mechanistic analyses showed that ADAMTS9, DCDC2, FAM46C, ZNF883, F2R, MSH6 and PAX2 genes may be potential downstream targets; DNA repair pathway and transcriptional regulation by TP53 pathway were involved. Finally, this study reveals that HIC1 is associated with lung cancer progression and may provide an effective strategy for its treatment. - Source: PubMed
Publication date: 2018/10/10
Li YueYao MengfeiWu TianqiZhang LiyanWang YingyingChen LiangFu GuohuiWeng XiaolingWang Jianhua - Tumor recurrence hinders treatment of ovarian cancer. The present study aimed to identify potential biomarkers for ovarian cancer recurrence prognosis and explore relevant mechanisms. RNA‑sequencing of data from the TCGA database and GSE17260 dataset was carried out. Samples of the data were grouped according to tumor recurrence information. Following data normalization, differentially expressed genes/micro RNAs (miRNAs)/long non‑coding (lncRNAs) (DEGs/DEMs/DELs) were selected between recurrent and non‑recurrent samples. Their correlations with clinical information were analyzed to identify prognostic RNAs. A support vector machine classifier was used to find the optimal gene set with feature genes that could conclusively distinguish different samples. A protein‑protein interaction (PPI) network was established for DEGs using relevant protein databases. An integrated 'lncRNA/miRNA/mRNA' competing endogenous RNA (ceRNA) network was constructed to reveal potential regulatory relationships among different RNAs. We identified 36 feature genes (e.g. TP53 and RBPMS) for the classification of recurrent and non‑recurrent ovarian cancer samples. Prediction with this gene set had a high accuracy (91.8%). Three DELs (WT1‑AS, NBR2 and ZNF883) were highly associated with the prognosis of recurrent ovarian cancer. Predominant DEMs with their targets were hsa‑miR‑375 (target: RBPMS), hsa‑miR‑141 (target: RBPMS), and hsa‑miR‑27b (target: TP53). Highlighted interactions in the ceRNA network were 'WT1‑AS‑hsa‑miR‑375‑RBPMS' and 'WT1‑AS‑-hsa‑miR‑27b‑TP53'. TP53, RBPMS, hsa‑miR‑375, hsa‑miR‑141, hsa‑miR‑27b, and WT1‑AS may be biomarkers for recurrent ovarian cancer. The interactions of 'WT1‑AS‑hsa‑-miR‑375‑RBPMS' and 'WT1‑AS‑hsa‑miR‑27b‑TP53' may be potential regulatory mechanisms during cancer recurrence. - Source: PubMed
Publication date: 2018/09/13
Wang XinHan LeiZhou LingWang LiZhang Lan-Mei