Ask about this productRelated genes to: Tcf7l2 Blocking Peptide
- Gene:
- TCF7L2 NIH gene
- Name:
- transcription factor 7 like 2
- Previous symbol:
- TCF4
- Synonyms:
- TCF-4
- Chromosome:
- 10q25.2-q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-20
- Date modifiied:
- 2018-02-13
Related products to: Tcf7l2 Blocking Peptide
Related articles to: Tcf7l2 Blocking Peptide
- Gastric cancer (GC) remains a leading cause of cancer-related deaths worldwide, with tumor stemness and metastasis driving poor prognosis. This study explores the role of eukaryotic translation initiation factor 4A1 (eIF4A1) in promoting these aggressive features in GC. eIF4A1 was found to be upregulated in stem-like (CD133) GC cells. Gain- and loss-of-function experiments in cell lines, combined with xenograft, chemically induced, and organoid models, demonstrated that eIF4A1 enhanced cancer stemness, cell mobility, tumorigenesis, and metastasis. Mechanistically, eIF4A1 selectively promotes p70 ribosomal S6 kinase (p70S6K) mRNA translation, leading to increased glycogen synthase kinase 3 beta (GSK3β) phosphorylation, elevated nuclear β-catenin accumulation, and subsequent transcriptional activation of eIF4A1 via the β-catenin/transcription factor 7-like 2 (TCF7L2) complex, thus forming a positive feedback loop. Clinically, high expression of eIF4A1, p70S6K, and TCF7L2 correlates with unfavorable prognosis in GC patients. These findings highlight eIF4A1 as a key regulator of stemness and metastasis through a novel translational feedback mechanism, suggesting potential therapeutic targeting to disrupt tumor progression. - Source: PubMed
Publication date: 2026/08/21
Su XiangyuZhu YingmingSong XueminYun ZhengchengHe YueqiWu YitingGao Chanchan - - Source: PubMed
Page Benjamin - Human Immunodeficiency Virus (HIV) infection impairs the immune system, diminishing its ability to defend against pathogens and increasing susceptibility to infections and diseases. To gain a comprehensive understanding of the heterogeneity, functions, and regulatory mechanisms of immune cells affected by different HIV viral loads, we investigated the biological impacts of HIV infection on the human body. We reanalyzed a publicly available peripheral blood mononuclear cell (PBMC) single-cell RNA sequencing dataset (GSE157829) comprising three people living with HIV with high viral load (HL-HIV), three people living with HIV with low viral load (LL-HIV), and one healthy control donor. We constructed single-cell immune atlases that represent different viral load profiles. We also analyzed the dynamic changes in specific immune cell subpopulations to gain insights into their signaling pathways, developmental trajectories, and key transcriptional regulators. At the single-cell level, non-classical monocyte subpopulations, specifically ncMono_LYN_TCF7L2 and ncMono_IL32, functioned as immunosurveillance elements but also activated pro-inflammatory pathways, leading to immune activation. B_CD83 subpopulation was critical in B cell development, facilitating B cell differentiation and tolerance. Naive.T_TNFAIP3 subpopulation exhibited anti-inflammatory effects and protected against aberrant apoptosis. Central memory T (TCM)_TCF7_CCR7 subpopulation played a crucial role in regulating the expansion of HIV-specific CD8 T cells and maintaining the immune response. Additionally, we observed a significant enrichment of IFI44L-positive subpopulations across different cell types, particularly in HL-HIV samples. Our findings demonstrate that HIV infection increases the complexity of immune cell subpopulations. Notably, IFI44L has emerged as a potential disease hub gene in HL-HIV samples, highlighting its potential as a novel biomarker for HIV. - Source: PubMed
Publication date: 2026/08/17
Gao JiaminLi YanjunHuang JinpingHuang XianzhenZhu QingdongWei CailingChen JielingLuo ShundaXie Zhouhua - Type 2 diabetes (T2D) is a multifactorial disorder arising from complex interactions between genetic susceptibility and environmental exposures, including diet. This systematic review aimed to synthesize and critically evaluate evidence on gene-diet interactions in T2D-related phenotypes among adults without diagnosed T2D at baseline. - Source: PubMed
Publication date: 2026/07/26
Kapellou AngelikiPapailia SevastianiFotis ThanasisVrachnos Dimitrios MiltiadisPapageorgiou DimitriosSalata EffieNtoumou EleniVittas Spiros - The transcription factor 7-like 2 () gene is one of the strongest genetic determinants of type 2 diabetes mellitus (T2DM), with the rs7903146 (C > T) polymorphism consistently associated with impaired insulin secretion and glucose dysregulation. This study investigated the associations between the rs7903146 polymorphism, glycemic control, oxidative stress biomarkers, and T2DM susceptibility, integrating bioinformatic analyses to explore the functional significance of this variant. This case-control study included 200 patients with T2DM, 100 prediabetic individuals, and 120 healthy controls. Genotyping of rs7903146 was performed using TaqMan SNP assays. Biochemical analyses included fasting plasma glucose (FPG), glycated hemoglobin (HbA1c), lipid profile, and oxidative stress biomarkers, including superoxide dismutase (SOD), glutathione peroxidase (GPx), total antioxidant capacity (TAC), and malondialdehyde (MDA). Bioinformatic analyses included population frequency analysis, regulatory annotation, chromatin accessibility assessment, expression quantitative trait locus (eQTL) analysis, protein interaction network construction, and pathway enrichment analyses to investigate the functional consequences of rs7903146. The T allele frequency was markedly higher in T2DM patients (33.5%) and prediabetic individuals (30%) than in controls (13.3%) ( < 0.001). T2DM susceptibility increased under allelic (OR = 3.27, 95% CI: 2.14-5.01), dominant (OR = 3.9, 95% CI: 2.37-6.42), and recessive (OR = 6.92, 95% CI: 1.59-30.07) models ( < 0.01). T2DM patients also showed significantly lower superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, lower total antioxidant capacity (TAC), and higher MDA levels ( < 0.001). T allele carriers had poorer glycemic control and greater oxidative stress. Bioinformatic analyses showed that rs7903146 resides within an active intronic regulatory region with chromatin accessibility, enhancer-associated histone marks, transcription factor occupancy, and candidate cis-regulatory elements. eQTL analyses showed tissue-specific effects on expression, while network and pathway analyses highlighted WNT signaling, β-catenin transcriptional complexes, and metabolic regulation and oxidative stress pathways. The TCF7L2 rs7903146 polymorphism was significantly associated with T2DM susceptibility, impaired glycemic regulation, and altered oxidative stress biomarkers. Bioinformatic analyses provided predictive evidence suggesting that rs7903146 may have tissue-specific regulatory relevance and may be indirectly linked to metabolic and WNT/β-catenin signaling pathways. However, because of the observational case-control design, these findings do not establish causality, and the proposed regulatory mechanisms require experimental validation. - Source: PubMed
Publication date: 2026/07/31
Ahmed Ahmed MAl-Nakhle Hakeemah HYousuf Amjad MEid Hamza M AMuddathir Abdel Rahim MAlsubhi Awadh SAljohani Hashim MAlhamawi Renad MTaher Mustafa YAlmalki FaisalAshour KholoudAlmutawif Yahya A