Ask about this productRelated genes to: TCF7L2 antibody
- 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 antibody
Related articles to: TCF7L2 antibody
- Negative affective signs are induced during withdrawal from acute opioid injection and increase in magnitude over repeated injections. Recent evidence indicates that opioid use also causes alterations in oligodendrocyte differentiation and myelination. To investigate these phenomena in mice, we examined spontaneous withdrawal following 10 days of oxycodone administration (30 mg/kg/day). Following a single injection, oxycodone increased exploratory locomotion and elevated thermal pain thresholds, consistent with the acute effect of opioid drugs. Twenty-four hours after oxycodone injection, mice interacted less in an open field, but did not differ from controls in the three-chamber social preference task. The following day (i.e., at the 48-h withdrawal point), oxycodone-withdrawn animals showed decreased marble burying. Tissue harvested from the medial prefrontal cortex (mPFC) after this test was analyzed for expression for 5 genes associated with regulation of oligodendrocyte cell lineage progression. RT-qPCR revealed decreased expression of Tcf7l2 and Klk6. These findings indicate behavioral and neurobiological alterations in response to oxycodone. The increased locomotion and antinociception seen following an acute oxycodone dose corroborates past rodent studies. Decreased marble burying during withdrawal represents a novel finding and may reflect anhedonia. The observed changes suggest that alterations in myelin-related gene expression accompany affective signs of acute withdrawal after repeated opioid exposure. - Source: PubMed
Publication date: 2026/06/12
Law Olivia MGewirtz Jonathan CVerpeut Jessica L - Our study investigated the association between transcription factor 7-like 2 (TCF7L2-rs7903146), angiotensin convertase enzyme (ACE-rs4646994), angiotensinogen (AGT-rs699), angiotensin II type 1 receptor (AGT1R-rs5186), fat mass and obesity-associated (FTO-rs17817499) and melanocortin 4 receptor (MC4R-rs17782313, rs12970134 and rs229616) single nucleotide polymorphisms (SNPs) with type 2 diabetes (T2D), obesity and hypertension in a Black South African population. - Source: PubMed
Publication date: 2026/06/10
Ngwa Ndonwi Elvisde Buys KerenMatshazi Don MakwakiweLevitt Naomi SLombard CarlDavison Glenda MaryMatsha Tandi EdithKengne Andre PascalHemmings Sian Megan JoannaPeer Nasheeta - The mechanisms by which Wnt/β-catenin signaling regulates gene expression in a tissue- and context-specific manner remain poorly understood, limiting our ability to target the aberrant cell growth typical of many Wnt-driven cancers. Here, we focus on malignant liver tumors driven by activating (β-catenin) mutations that nevertheless display distinct phenotypic states and Wnt outputs. By profiling patient-derived organoids via single-cell transcriptomics and chromatin dynamics, we identify subtype-specific transcriptional and epigenetic profiles. Using CUT&RUN, we show that β-catenin engages distinct genomic regions, dictated by differential association with TCF/LEF family transcription factors. Specifically, we define a sequence-specific regulatory element engaged by β-catenin only upon interaction with TCF7L2, revealing that partner choice, independent of mutational status, ultimately determines cell fate. Our findings, validated across multiple tumor models and patient tissues, offer a framework for understanding how differential β-catenin-TCF/LEF interaction orchestrates context-specific Wnt signaling outcomes. - Source: PubMed
Publication date: 2026/06/10
Kluiver Thomas ANordin AnnaLu YuyanGuo XuanSchubert Stephanie AYeung DarienArdisasmita Arif IbrahimTerpstra WesselZhang ChangDuan XiaochenSavur Rishivan den Heuvel Marius Cde Meijer Vincent Ede Kleine Ruben HKraal Kathelijnede Krijger Ronald RZsiros JózsefCantù ClaudioPeng Weng Chuan - Loss of the chromatin remodeler WSTF (BAZ1B), a gene deleted in Williams syndrome, causes reproducible, genome-scale reprogramming of chromatin states and transcript processing that links altered chromatin composition to misprocessed transcripts and aberrant signaling. Using engineered HCT116-WSTFKO cells, we combine transcriptome profiling, microscopy, chromatin CUT&RUN, and histone post-translational modification (HPTM)-defined chromatin state modeling to show that WSTF localizes to promoters and gene bodies of actively transcribed loci together with ASH2L and CBP. Loss of WSTF causes depletion of ASH2L/CBP, selective loss of H3K4me2 and multiple acetylation marks, and gain of Polycomb components. This loss results in systematic conversion from a multi-mark active promoter/enhancer chromatin landscape to a hypoacetylated, H3K4me2-depleted, PRC-enriched landscape. These chromatin changes coincide with widespread isoform switching and splicing alterations in genes encoding chromatin regulators and signaling pathways. This WSTF deficiency produces Wnt/β-catenin hyperactivation. A locus-specific example at TCF7L2 demonstrates how gene body loss of active marks drives isoform switching that alters DNA binding domains and decouples stabilized nuclear β-catenin from canonical target engagement. Our results establish a mechanistic chain from WSTF-dependent chromatin architecture to co-transcriptional RNA processing integrity, signaling pathway fidelity, and developmental gene program regulation relevant to Williams syndrome. - Source: PubMed
Behrouz Sharif ShahinDennis Jonathan H - Behavioral and phenotypic characteristics do not fully explain variability in African Americans with youth-onset type 2 diabetes (Y-T2D) treated with metformin with or without liraglutide. We hypothesized that biological heterogeneity, including genetic variation in the metformin transporter influences metformin pharmacokinetics and hepatic glucose flux. Therefore, we sought to characterize metformin pharmacokinetics in Y-T2D and evaluate genetic variants known to modulate metformin efficacy in adults to determine the mechanisms underlying variation in treatment response. - Source: PubMed
Publication date: 2026/05/28
Cantor Samson LZeng YiDavis Faith SGlaros Sophia BMacheret Natalie AKacker Ila NMalandrino NoemiMabundo LilianArisa Oluwatobi TAdeyemo Adebowale ACai HongyiCourville Amber BShouppe Eileen LWalter Mary FWalter Peter JRotimi Charles NFigg William DBentley Amy RChung Stephanie T