Ask about this productRelated genes to: TINAGL1 antibody
- Gene:
- TINAGL1 NIH gene
- Name:
- tubulointerstitial nephritis antigen like 1
- Previous symbol:
- LCN7
- Synonyms:
- P3ECSL, LIECG3, ARG1, TINAGRP
- Chromosome:
- 1p35.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-29
- Date modifiied:
- 2016-10-05
Related products to: TINAGL1 antibody
Related articles to: TINAGL1 antibody
- Dementia with Lewy Bodies (DLB) is the most common neurodegenerative dementia after Alzheimer's disease (AD), but it remains challenging to diagnose due to overlapping symptoms and mixed pathologies. This pilot study tested whether DLB has different metabolic blood proteomic profiles compared to AD and controls. Serum was analysed from people with DLB ( = 20), a group with AD (either with Alzheimer's disease dementia or Mild Cognitive Impairment with a positive amyloid positron emission tomography scan (MCI+/AD) ( = 15), and similarly aged controls ( = 15) using the Olink Metabolism panel encompassing 92 proteins. Six proteins (PILRB, LRIG1, NECTIN2, TINAGL1, SSC4D, and FKBP4) were significantly different in DLB compared with the controls, and one protein (SERPINB8) was differentially expressed when compared with MCI+/AD. Receiver operating characteristic curves for biologically relevant proteins that have previously established roles in neurodegenerative and cognitive properties showed that RNASE3 levels could differentiate DLB from MCI+/AD (area under the curve (AUC) = 0.717, sensitivity = 0.850, and specificity = 0.600). A multimarker model incorporating RNASE3 with phosphorylated tau 217 (pTau217) and polygenic risk scores for LBD achieved improved accuracy in discriminating DLB from MCI+/AD (AUC = 0.963, sensitivity = 1.000, and specificity = 0.900). Pathway analyses revealed dysregulation in cortisol signalling, inflammation resolution, and ErbB4-mediated neuroplasticity, which point towards peripheral protein alterations related to the adaptation to stress, immune regulation, and synaptic integrity in DLB. The present exploratory study highlights potential pathophysiological mechanisms implicated in DLB, suggesting that a multimodal biomarker panel may perform better compared to single proteins. Considering the small sample sizes, the findings will need to be replicated in larger cohorts. - Source: PubMed
Publication date: 2026/07/31
Pritha Ariana NChouliaras LeonidasSwann PeterPrats-Sedano MariaMcKeever AnnaHeslegrave AmandaAshton Nicholas JZetterberg HenrikSu LiMalpetti MauraRowe James BO'Brien John T - Longitudinal proteomic studies on hypertension remain scarce. We evaluated the epidemiological associations of circulating proteins with hypertension on the basis of the UK Biobank (UKB) and public GWAS-summary data in this study. - Source: PubMed
Publication date: 2026/05/07
Zhang HongruiLiang ZhuoshuaiHu XinmengJin HuizhenZhang YuanWang JiaheYu BowenTian YuyangQiu ShuangLi YongGu YuluLiu YunkaiCheng YiShi JikangLiu Yawen - Emerging omics approaches, including metabolomics and proteomics, can be integrated into obesity treatment for better blood pressure management. We tested whether preoperative metabolomic and proteomic profiles predict long-term elevated blood pressure (EBP) changes better than known risk factors in adolescents undergoing bariatric surgery. - Source: PubMed
Publication date: 2025/10/20
Pan ShudiLi ZhenjiangLewinger Juan PabloGoodrich Jesse AWang HongxuRock SarahChen CarmenJenkins Todd MSisley StephanieDaniels Stephen RWalker Douglas IAung Max TGarcia ErikaMcConnell RobEckel Sandrah PLa Merrill Michele AAlderete Tanya LChen ZhuanghuaGilliland Frank DInge Thomas HConti David VRyder Justin RChatzi Lida - The intestinal epithelium is frequently exposed to environmental contaminants such as fumonisins, mycotoxins implicated in the development of mycotoxicosis across various mammalian species, with fumonisin B (FB) being the most prevalent and toxic congener. Fumonisin B (FB) can be enzymatically hydrolysed to produce hydrolysed fumonisin B (HFB) that displays reduced inhibitory activity toward ceramide synthase. Given the central role of ceramide synthase in sphingolipid metabolism and cellular homeostasis, the reduced inhibitory activity of HFB is considered toxicologically favourable, as it is less likely to disrupt membrane integrity and critical signalling pathways. However, the toxicity of HFB remains variable across different in vitro and in vivo models. In this study, we evaluated the impact of FB and HFB on cell viability, apoptosis, and proliferation in the porcine intestinal cell line (IPEC-J2), including inflammatory responses through interleukin 8 (IL-8). Molecular mechanisms and pathways influenced by FB and HFB exposure were investigated through proteomic and bioinformatic analyses. Differentially abundant proteins (DAPs) were identified and functionally characterised using Gene Ontology analysis based on the Sus scrofa (domestic pig) database, revealing 52 significant DAPs between FB and HFB treatments compared to the control. Fibronectin 1 (FN1), an adhesive glycoprotein of the intestine, was consistently detected as a DAP in cells exposed to FB and HFB. FB upregulates FN1, while HFB downregulates it, leading to different oncogenic pathways revealed by STRING enrichment analysis. Proteomic analysis further revealed distinct DAPs following FB and HFB exposure, implicating alterations in immune modulation (e.g. differential regulation of CD276), iron homeostasis (upregulation of FTL and FTH1), epithelial integrity (downregulation of NTN4, ST14), extracellular matrix remodelling (reduced SPARC), and angiogenesis-related pathways (decreased TINAGL1, FBLN2, SDC4) suggesting early changes in cellular signalling, stress response, and structural regulation that may be relevant to cancer biology and warrant further investigation. These findings also demonstrate that HFB activates distinct cancer-related pathways in vitro compared to FB, with in vivo studies suggesting divergent mechanisms. HFB also induces more extensive protein expression changes in IPEC-J2 cells, as reflected by the greater number of DAPs and the complexity of enriched pathways. However, further investigation is needed to determine whether these changes directly contribute to cytotoxicity or represent compensatory cellular responses. - Source: PubMed
Publication date: 2025/10/09
Gamiet NabeelaDeepnarain NashiaAbel StefanBurger Hester-MariMayer ElisabethLilly Mariska - Adenylate uridylate-rich element genes (AREGs) are crucial in modulating gene expression following transcription. However, the comprehensive role of AREGs in lung squamous carcinoma (LUSC) r emains inadequately understood. Transcriptome data from TCGA and GTEx databases to identify differentially expressed AREGs. Clustering algorithms were used to identify AREGs-related subtypes, and a prognostic model was developed through univariate/multivariate and LASSO regression analyses. Following this, we created a nomogram integrating clinical pathologic characteristics and the risk model. The immune microenvironment was evaluated using CIBERSORT, ESTIMATE, and MCPcounter analyses. We examined the mRNA expression of the signature genes in normal and lung squamous carcinoma cells using RT-qPCR. Finally, we assessed the sensitivity to drugs based on the signature genes in risk patients. Patients with the 2 identified molecular subtypes exhibit distinct prognoses and immune microenvironments. We identified 5 genes with prognostic significance that can serve as independent predictors in clinical practice. The low-risk patients demonstrates more favorable prognostic outcomes, while the high-risk patients show elevated immune scores and increased immune cell infiltration, suggesting a favorable response to immunotherapy. RT-qPCR results showed upregulation of FAM83A and TINAGL1 and downregulation of FGG and ADH1C in LUSC. In addition, the low-risk patients show increased sensitivity to vinorelbine. The molecular subtypes and prognostic model based on AREGs demonstrate reliable clinical prognostic value. This finding may contribute to personalized and precise treatment for patients with LUSC, offering new insights for improving patient outcomes. - Source: PubMed
Publication date: 2026/05/01
Huang JunchaoChen SiyangLiu Yakun