TCF4 antibody - N-terminal region (P100775_P050)
- Known as:
- TCF4 (anti-) - N-terminal region (P100775_P050)
- Catalog number:
- p100775_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TCF4 antibody - N-terminal region (P100775_P050)
Related genes to: TCF4 antibody - N-terminal region (P100775_P050)
- Gene:
- TCF4 NIH gene
- Name:
- transcription factor 4
- Previous symbol:
- -
- Synonyms:
- SEF2-1B, ITF2, bHLHb19, E2-2
- Chromosome:
- 18q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-10-16
- Date modifiied:
- 2018-06-28
- 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: TCF4 antibody - N-terminal region (P100775_P050)
Related articles to: TCF4 antibody - N-terminal region (P100775_P050)
- Most pregnancies are affected by nausea and vomiting, but the most severe form-hyperemesis gravidarum-can be life threatening. Here we performed a multi-ancestry genome-wide association study of hyperemesis gravidarum in 10,974 cases and 461,461 controls across European, Asian, African and Latino ancestries. We identified ten associations: four identified previously (GDF15, IGFBP7, PGR and GFRAL) and six additional loci (SLITRK1, SYN3, IGSF11, FSHB, TCF7L2 and CDH9). Downstream analyses revealed GDF15 and TCF7L2 expression primarily in extravillous trophoblasts, with opposing effects for GDF15 between maternal and fetal genotype. Conversely, IGFBP7 and PGR were expressed primarily in maternal spiral arteries, with effects limited to the maternal genome. Selected loci were associated with abnormal pregnancy weight gain, duration, birth weight and pre-eclampsia. Functional studies identified additional associations including antisense IGFBP7-AS1 and protein ACP1. Potential roles for candidate genes in appetite, insulin signaling and brain plasticity provide pathways to explore etiological mechanisms and therapeutic avenues. - Source: PubMed
Publication date: 2026/04/14
Fejzo MarlenaWang XinranTan QingZöllner JuliaPujol-Gualdo NatàliaLaisk Triin Finer Sarahvan Heel David A Brumpton BenBhatta LaxmiHveem KristianJasper Elizabeth AVelez Edwards Digna RHellwege Jacklyn NEdwards ToddJarvik Gail PLuo YuanKhan AtlasMacGibbon KimberGao YuanGe GaoxiangAverbukh InnaSoon ErinAngelo MichaelMagnus PerJohansson StefanNjølstad Pål RKim ArtemGazal StevenVaudel MarcShu Chang AprilMancuso Nicholas - Preeclampsia (PE), a pregnancy complication, affects 10% of pregnancies worldwide. The develop-ment of PE has been attributed to multiple genetic variations. The aim of this study was to evaluate the possible association between TCF7L2 gene polymorphisms (rs12255372 and rs12243326) and risk of preeclampsia in Egyptian women with and without gestational diabetes mellitus (GDM) as well as to assess the discrimination values of these polymorphisms as biomarkers for PE. - Source: PubMed
Ellithy ShaimaaGouda WeaamMageed LamiaaOkasha AhmedAfify Mie - Proteolysis-targeting chimera (PROTAC) therapies degrading SWI/SNF ATPases interfere with androgen receptor (AR) signaling in AR-dependent castration-resistant prostate cancer (CRPC-AR). To explore the utility of SWI/SNF therapy beyond AR-sensitive CRPC, we investigated SWI-/SNF-targeting agents in AR-negative CRPC. SWI-/SNF-targeting PROTAC treatment of cell lines and organoid models reduced the viability of not only CRPC-AR but also WNT signaling-dependent AR-negative CRPC (CRPC-WNT). The CRPC-WNT subgroup represents 11% of around 400,000 cases of CRPC worldwide that die yearly. SWI/SNF ATPase SMARCA4 depletion interfered with the master transcriptional regulator TCF7L2 in CRPC-WNT. Functionally, TCF7L2 maintained proliferation via the MAPK signaling axis in this subtype of CRPC. Together, these data provide a mechanistic rationale for interventions that perturb DNA binding of the proproliferative transcription factor TCF7L2 and/or direct MAPK signaling inhibition in the CRPC-WNT subclass of advanced prostate cancer. - Source: PubMed
Thienger PhillipPaassen IreneYao XiaosaiRubin Philip DLehner MarikaLillis NicholasBenjak AndrejShah Sagar RLeung Alden King-Yungde Brot SimoneNaveed AlinaDaniel BenceShi MinyiTremblay JulienTriscott JoannaCassanmagnago Giada AndreaBolis MarcoMela LiaBeltran HimishaChen YuPiscuoglio SalvatoreYu HaiyuanNg Charlotte K YQuigley David AYauch Robert LRubin Mark A - Type 2 diabetes (T2D) is a heterogeneous metabolic disorder. Recent cluster-based classifications offer insights into distinct pathophysiological subtypes. The objective of the study is to investigate the association of genetic variants in T2D-related genes with defined T2D clusters. We analyzed 678 single nucleotide polymorphisms (SNPs) from ten genes (CDKAL1, CDKN2A, CDKN2B, HHEX, KCNQ1, MTNR1B, PAX4, SLC30A8, TCF7L2, and UBE2E2) in 471 T2D patients classified into four clusters: Severe Insulin-Deficient Diabetes (SIDD), Mild Obesity-related Diabetes (MOD), Mild Age-related Diabetes (MARD), and Metabolic Syndrome-related Diabetes (MSD). Genotyping was performed using the Axiom PDMRAv2 array. Following Hardy-Weinberg Equilibrium filtering, 376 SNPs were analysed. The association between T2D clusters and SNPs was assessed by multinomial logistic regression. Nineteen SNPs showed significant differences in genotypic frequencies among clusters (p < 0.05). Eight SNPs (rs61875103 in TCF7L2; rs12576156, rs2283220, rs2074197, and rs163165 KCNQ1; rs4710943, rs9368248, and rs6456379 in CDKAL1) significantly associated with cluster assignment. Cluster-specific effects were most notable in SIDD and MOD subgroups. Our findings support genetic heterogeneity of TCF7L2, KCNQ1, and CDKAL1 in T2D clusters and underscore the potential for genetically informed precision therapy strategies. - Source: PubMed
Publication date: 2025/12/20
Plengvidhya NattachetTeerawattanapong NipapornNarkdontr TassaneeInnang SaranyaSonglilitchuwong SuavalukSuthon SarochaTangjittipokin Watip - Hypoxia plays a crucial role in the advancement of colorectal cancer (CRC); however, the downstream mechanisms facilitated by hypoxia-inducible factor 1α (HIF-1α) remain incompletely understood. This study employed in vitro and in vivo models to investigate the role of transcription factor 7-like 2 (TCF7L2) under hypoxic conditions in CRC. Utilizing reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis, we observed an upregulation of TCF7L2 mRNA and protein expression in Caco-2 and HCT-116 CRC cell lines under hypoxia. Functional assays, including CCK-8, colony and sphere formation, Transwell, flow cytometry, and xenograft tumor models, provided evidence that the knockdown of TCF7L2 leads to the suppression of CRC cell proliferation, the induction of apoptosis, cell cycle arrest at the G0/G1 phase, and a decrease in migration and invasion capabilities. Furthermore, it inhibited epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) characteristics in vitro, while also reducing tumor growth in vivo. Mechanistically, chromatin immunoprecipitation (ChIP) and co-immunoprecipitation (co-IP) assays have elucidated that the expression of TCF7L2 induced by hypoxia is dependent on HIF-1α, which directly binds to hypoxia response elements (HREs) within the TCF7L2 promoter. Additionally, Western blot and experiments employing the PI3K inhibitor LY294002 have demonstrated that TCF7L2 activates the PI3K/AKT signaling pathway, thereby facilitating the proliferation of CRC cells. A clinical analysis of 104 CRC specimens, utilizing immunohistochemistry (IHC) and RT-qPCR, revealed that elevated expression levels of TCF7L2 were significantly associated with advanced T stage, metastasis, and unfavorable prognosis. Spearman correlation analysis confirmed a positive relationship between the expressions of TCF7L2 and HIF-1α, while Kaplan-Meier survival analysis demonstrated that their co-expression was predictive of reduced overall survival. Collectively, these findings position TCF7L2 as a critical downstream effector of HIF-1α in hypoxic CRC, and its mechanistic role in promoting malignancy and correlation with poor prognosis provide a theoretical basis for exploring TCF7L2 as a potential therapeutic target in future studies. - Source: PubMed
Publication date: 2025/12/18
Tang KangCheng YongGong JianpingLi Yang