Ask about this productRelated genes to: Tead4 antibody
- Gene:
- TEAD4 NIH gene
- Name:
- TEA domain transcription factor 4
- Previous symbol:
- TCF13L1
- Synonyms:
- TEF-3, TEFR-1, EFTR-2, RTEF-1
- Chromosome:
- 12p13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1996-08-02
- Date modifiied:
- 2016-01-15
Related products to: Tead4 antibody
Related articles to: Tead4 antibody
- The overexpression of the transcriptional enhanced associate domain (TEAD), which regulates gene transcription linked to cell growth, drives the proliferation in cases of hepatocellular carcinoma (HCC). In order to discover novel TEAD inhibitors that are more effective and have better efficacy and pharmacokinetic properties for treating HCC, this study employed a cyclization strategy to generate a novel indole-based scaffold of TEAD inhibitors. A comprehensive and systematic structure-activity relationship (SAR) analysis identified the most promising compound: LC-TD-05, a non-covalent, partial TEAD inhibitor with selective activity against TEAD1, TEAD2 and TEAD4, but reduced potency against TEAD3. LC-TD-05 exhibits good potency against TEAD1/2/4 (TEAD1 IC = 116.6 ± 21.7 nM, TEAD2 IC = 168.7 ± 17.1 nM, TEAD4 IC = 68.3 ± 18.2 nM), demonstrates favorable oral bioavailability (F = 53.7%), and exhibits significant anti-tumor activity in HCC LM3 models in vitro (LM3 cell IC = 248 ± 27.9 nM) and in vivo (TGI = 75%). Overall, this study provides a novel scaffold for TEAD inhibitors, enabling more effective interventions against HCC. - Source: PubMed
Publication date: 2026/04/30
Xu DounanSu WenxiMiao YuhuiLuo XiaolinLuo YipanHu ShuangWang YongpengHu ChujiaoLuo ChengLi GuangmingZhang YuanyuanChen ShijieXiong Huan - During preimplantation development, mammalian embryos form blastocysts. Studies in mouse embryos have revealed multiple roles of the Hippo signaling pathway in this process. Among them, the process of TEA domain transcription factor 4 (TEAD4)-Yes-associated protein (YAP) control of trophectoderm (TE) and inner cell mass fate is the most extensively characterized. The major mechanism of YAP regulation is the activation of Hippo signaling by adherens junctions and inhibition by cell polarization or the apical domain. Several additional mechanisms further modulate Hippo signaling and/or YAP, including polarity regulation by Rho-associated coiled-coil-containing protein kinase (ROCK) and transcription factor AP-2γ (TFAP2C), angiomotin (AMOT) regulation by Ras homolog (RHO), asymmetric inheritance of the apical domain, mechanical regulation, and glucose metabolism. Hippo signaling also regulates other processes during embryogenesis, including zygotic gene activation by maternal YAP, cell state transition at the 8-cell stage, and maturation and quality control of the epiblast via cell competition. The TE fate regulatory role of the Hippo pathway is evolutionarily conserved among mammalian species, including human and bovine embryos, but some details differ. - Source: PubMed
Publication date: 2026/04/17
Sasaki Hiroshi - Hepatocellular carcinoma (HCC) is a deadly malignancy marked by frequent metastasis and recurrence. Despite therapeutic advances, HCC metastasis and immune evasion remain major hurdles to effective treatment. Here, by analyzing clinical HCC specimens, we found that levels of ubiquitin-fold modifier 1 conjugation (UFMylation), a ubiquitin-like modification, correlated with prognosis, pathological features, and metastatic burden. Emerin (EMD), a nuclear envelope protein, was identified as a UFMylation substrate. Loss of UFMylation destabilized EMD via proteasomal degradation, promoting nuclear β-catenin accumulation and hybrid epithelial-mesenchymal transition (EMT), enhancing tumor cell migration, invasion, circulating tumor cell formation, and extravasation. Nuclear β-catenin also interacted with TEAD4 to upregulate poliovirus receptor (PVR), enabling natural killer (NK) cell evasion via the PVR-TIGIT axis. Reduced UFMylation accelerated metastasis in models of HCC, as well as colorectal cancer (CRC), while EMD restoration mitigated these effects. Combined PD-1 and TIGIT blockade significantly suppressed tumor growth and metastasis in UFMylation-deficient settings. Together, these data suggest that UFMylation suppresses HCC and CRC metastasis by stabilizing EMD, thereby inhibiting β-catenin-driven hybrid EMT and PVR-mediated immune evasion. These preclinical findings suggest that activating the UFMylation axis may have therapeutic potential for metastatic HCC. - Source: PubMed
Publication date: 2026/04/17
Xu MinGao XukangZhao JieXu DongweiMa ChenchaoFan MingmingLin JianboKong XiaoniZhao ZhicongLi MengLiu Shaoqing - Aberrant interplay between epigenetics and metabolism contributes to prostate cancer (PCa) progression and represents a formidable challenge limiting the efficacy of drugs. Elucidation of the epigenetic underpinnings of prostate cancer (PCa) could provide promising insights into the drivers of therapy resistance. Through an unbiased siRNA screen of mSWI/SNF family members, which play a significant role in tumorigenesis, we identified Bromodomain containing 9 (BRD9) as an essential gene for PCa growth. Targeting BRD9 abolished PCa colony formation and migration in vitro, and inhibited orthotopic tumor growth in vivo. YAP/TEAD4 complex bound to the BRD9 promoter to elevate its levels. Integrated CUT&Tag-seq and RNA-seq analyses revealed DGAT1 as an important BRD9 effector. Mechanistically, BRD9 interacted with SREBP1 to co-occupy the DGAT1 promoter, increasing the H3K4me3 enrichment and chromatin accessibility. Additionally, the YAP-BRD9 axis enhanced the lipid droplets (LDs) formation, ferroptosis resistance, and tumorigenesis via inducing DGAT1. The pharmacological inhibition (or depletion) of BRD9 suppressed LDs formation, restored ferroptosis sensitivity, and PCa malignancy. Overall, the BRD9-SREBP1-DGAT1 axis represents a potential epigenetic therapeutic target for YAP-high PCa. - Source: PubMed
Publication date: 2026/04/14
Zhu XuejinWen ZhimeiWu JinhaiChen SianXu RanWang BinZhu YingwenChen Yanfei - The Hippo pathway, a highly conserved kinase signaling cascade, is central to regulating cell growth and proliferation, tissue homeostasis, and organ development. As downstream effectors of this pathway, TEAD1-4 proteins serve as sequence-specific transcription factors in mammals. They collaborate with cofactors, such as VGLL and YAP/TAZ, to modulate gene expression, thereby controlling diverse cellular processes. Here, employing fluorescence-combined optical tweezers, we demonstrate that monomeric TEAD4 binds to consensus motifs with association rates significantly higher than nonspecific DNA, while the dissociation rates are fast and comparable. Yet, TEAD4, through multimerization, gains multiple DNA binding sites, supporting elongated DNA residence time and YAP recruitment. Moreover, both YAP and VGLL4 can promote TEAD4 multimerization and strengthen its DNA binding and sequence specificity. Unexpectedly, the presence of two Tondu domains in VGLL4 elicits a stoichiometry-dependent effect on YAP recruitment to DNA-bound TEAD4: A low VGLL4:TEAD4 molar ratio enhances this process, whereas a high ratio inhibits it. These findings offer a dynamic understanding of how a eukaryotic TF interacts with DNA and underscore a distinct molecular mechanism by which VGLL4 modulates TEAD4-mediated YAP recruitment in the Hippo pathway. - Source: PubMed
Publication date: 2026/04/11
Ren ZhiyunZhao YilinYu WentaoZhang XiaSong XiaoxuanBao YanlingHu MengChen LishuangYang HaoCheng BingkaiLiu CongJin YunyunZhang LeiSun Bo