Ask about this productRelated genes to: YIPF2 Blocking Peptide
- Gene:
- YIPF2 NIH gene
- Name:
- Yip1 domain family member 2
- Previous symbol:
- -
- Synonyms:
- MGC3262, FinGER2
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-04
- Date modifiied:
- 2019-03-21
Related products to: YIPF2 Blocking Peptide
Related articles to: YIPF2 Blocking Peptide
- This study identifies diagnostic biomarkers of OA-related synovitis from synovial tissue expression and develops a validated diagnostic nomogram (differentially expressed genes = differentially expressed genes; single-sample gene set enrichment analysis [ssGSEA]). We analyzed GEO synovium datasets (training: GSE55235, GSE55457, GSE82107, OA = 30 vs controls = 27; validation: GSE89408, OA = 22 vs controls = 28; cartilage comparator: GSE129147, OA = 10 vs controls = 9) and applied weighted gene correlation network analysis to identify phenotype-linked modules, followed by 4 machine learning models (random forest [RF], support vector machine [SVM], xtreme gradient boosting (XGB), generalized linear model [GLM]) to rank genes, selection of hub genes from the top SVM features, construction and validation of a multigene nomogram predicting OA-related synovitis vs control, and integrative pathway and immune profiling (gene ontology/kyoto encyclopedia of genes and genomes, ssGSEA), competitive endogenous RNA network analysis, and hypothesis-generating protein-ligand docking. In the training synovium set (GSE55235 + GSE55457 + GSE82107; outcome = OA-related synovitis vs control), model area under the curves (AUCs; 95% confidence intervals) were RF 0.944 (0.882-1.000), SVM 1.000 (0.997-1.000), XGB 0.917 (0.842-0.992), and GLM 0.944 (0.882-1.000). In the external synovium validation dataset GSE89408 (outcome = OA-related synovitis vs control), AUCs (95% confidence intervals) were RF 0.729 (0.585-0.873), SVM 0.792 (0.662-0.922), XGB 0.717 (0.571-0.863), and GLM 0.771 (0.636-0.906), emphasizing external validation as the fairer test of model generalizability. The cartilage comparator GSE129147 (outcome = OA vs control in cartilage) yielded SVM AUC 0.833 (0.333-1.000), supporting tissue-specific yet cross-tissue consistency. Five hub genes - CTSH, ephrin-B2, YIPF2, ZNF671, SLC27A6 - were identified from 462 intersecting genes, selected from the SVM model because it showed the smallest residuals and best internal discrimination among the 4 tested algorithms. The 5-gene nomogram showed good calibration and decision-curve net benefit across 10% to 40% threshold probabilities, confirming its diagnostic utility. ssGSEA analysis revealed enriched immune-related pathways and higher infiltration of B cells, macrophages, mast cells, and T-cell subsets in OA synovium, closely associated with the expression of hub genes such as YIPF2 and ZNF671 linked to adaptive-immune and inflammatory signaling. Molecular docking indicated that dexamethasone and triamcinolone acetonide bind to the protein products of the hub genes (-7.1 to -8.5 kcal/mol). The 5-gene synovium-based SVM model provides a validated diagnostic nomogram for OA-related synovitis; docking findings are hypothesis-generating and not evidence of therapeutic efficacy. - Source: PubMed
Wang PengJiang XingwenXia XiaofengZou KaiZuo BinHe Jingxuan - Understanding of the mechanisms for genome integrity maintenance can help in developing effective intervention strategies to combat aging. A whole-genome RNAi screen was conducted to identify novel factors involved in maintaining genome stability. The potential target genes identified in the screening are related to the cell cycle, proteasome, and spliceosomes. Unexpectedly, the Golgi protein YIPF2 has been found to play a critical role in maintaining genome stability. The depletion of YIPF2 hinders the process of homologous recombination (HR) repair, which then triggers DNA damage response mechanisms, ultimately leading to cellular senescence. The overexpression of YIPF2 facilitated cellular recovery from DNA damage induced by chemotherapy agents or replicative senescence-associated DNA damage. Our findings indicate that only the intact Golgi apparatus containing YIPF2 provides a protective effect on genome integrity. - Source: PubMed
Publication date: 2024/09/05
Zhang XiaoWang Tao - Excessive secretion of human islet amyloid polypeptide (hIAPP) is an important pathological basis of diabetic encephalopathy (DE). In this study, we aimed to investigate the potential implications of hIAPP in DE pathogenesis. Brain magnetic resonance imaging and cognitive scales were applied to evaluate white matter damage and cognitive function. We found that the concentration of serum hIAPP was positively correlated with white matter damage but negatively correlated with cognitive scores in patients with type 2 diabetes mellitus. In vitro assays revealed that oligodendrocytes, compared with neurons, were more prone to acidosis under exogenous hIAPP stimulation. Moreover, western blotting and co-immunoprecipitation indicated that hIAPP interfered with the binding process of monocarboxylate transporter (MCT)1 to its accessory protein CD147 but had no effect on the binding of MCT2 to its accessory protein gp70. Proteomic differential analysis of proteins co-immunoprecipitated with CD147 in oligodendrocytes revealed Yeast Rab GTPase-Interacting protein 2 (YIPF2, which modulates the transfer of CD147 to the cell membrane) as a significant target. Furthermore, YIPF2 inhibition significantly improved hIAPP-induced acidosis in oligodendrocytes and alleviated cognitive dysfunction in DE model mice. These findings suggest that increased CD147 translocation by inhibition of YIPF2 optimizes MCT1 and CD147 binding, potentially ameliorating hIAPP-induced acidosis and the consequent DE-related demyelination. - Source: PubMed
Publication date: 2024/07/29
Zhang NanMa XiaoyingHe XinyuZhang YaxinGuo XinShen ZhiyuanGuo XiaosuZhang DanshenTian ShujuanMa XiaoweiXing Yuan - Venous thromboembolism (VTE) is known to be intricately linked to severe COVID-19 (sCOVID-19) occurrence. Herein, we employed univariable Mendelian randomization (MR) and transcriptome analysis to predict the causal association and associated signaling networks between VTE and sCOVID-19. - Source: PubMed
Publication date: 2024/04/29
Chen LiangDai Xiaoting - Non-small cell lung cancer (NSCLC) is the most common histological type of lung cancer, and the identification of the apoptotic process of NSCLC is vital for its treatment. Usually, both the expression level and the cell surface level of TNFRSF10B (TNF Receptor superfamily member 10B) will increase after treatment with some chemotherapeutic agents, which plays a critical role in the apoptosis induction. However, the exact molecular mechanism underlying TNFRSF10B regulation remains largely elusive. Here, we found that TNFRSF10B, along with a vesicular trafficking regulator protein, YIPF2, were upregulated after treatment with pemetrexed (PEM) in NSCLC cells. Besides, YIPF2 increased the surface level of TNFRF10B, while YIPF2 knockdown inhibited the upregulation of TNFRSF10B and its recycling to plasma membrane. In addition, RAB8 decreased the cell surface TNFRSF10B by promoting its removing from plasma membrane to cytoplasm. Furthermore, we found that YIPF2, RAB8 and TNFRSF10B proteins interacted physically with each other. YIPF2 could further inhibit the physical interaction between TNFRSF10B and RAB8, thereby suppressing the removing of TNFRSF10B from plasma membrane to cytoplasm mediated by RAB8 and maintaining its high level on cell surface. Finally, using bioinformatics database, the YIPF2-TNFRSF10B axis was confirmed to be associated with the malignant progression of lung cancer. Taken together, we show that YIPF2 promotes chemotherapeutic agent-mediated apoptosis via enhancing TNFRSF10B recycling to plasma membrane in NSCLC cells. These findings may be beneficial for the development of potential prognostic markers of NSCLC and may provide effective treatment strategy. - Source: PubMed
Publication date: 2020/04/17
Wang YingyingGuo SenLi DongmeiTang YongkangLi LeiSu LingLiu Xiangguo