Affinage

TEAD1

Transcriptional enhancer factor TEF-1 · UniProt P28347

Length
426 aa
Mass
47.9 kDa
Annotated
2026-04-28
100 papers in source corpus 36 papers cited in narrative 36 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TEAD1 is a TEA domain transcription factor that binds M-CAT DNA elements to regulate tissue-specific gene programs governing cardiac contractility, vascular smooth muscle differentiation, skeletal muscle homeostasis, Schwann cell myelination, and cell proliferation across multiple lineages. It functions as the principal nuclear effector of Hippo pathway signaling by partnering with co-activators YAP, TAZ, and VGLL family members through a conserved C-terminal binding pocket, while also exerting YAP/TAZ-independent transcriptional repression—recruiting co-repressors VGLL4 and MENIN or directly interfering with RNA Polymerase II loading at target promoters (PMID:36484096, PMID:36662616, PMID:15628970, PMID:12376544). In cardiomyocytes, TEAD1 directly activates SERCA2a, Inhibitor-1, and nuclear-encoded mitochondrial genes; its loss triggers mitochondrial dysfunction and necroptosis-driven dilated cardiomyopathy (PMID:28878117, PMID:33469230). A Y421H missense mutation that selectively abolishes YAP/TAZ binding causes Sveinsson's chorioretinal atrophy, and TEAD1 activity is further tuned by RBFOX2/hnRNPU-regulated alternative splicing of exon 5/6 and by SUMO1 conjugation at K173, which modulates protein stability, nuclear retention, and YAP interaction strength (PMID:15016762, PMID:17689488, PMID:35699208, PMID:38670107, PMID:38225750).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1994 High

    Establishing that TEAD1 isoforms bind M-CAT elements with high affinity but differ in transcriptional activation capacity resolved how a single gene could produce both activating and non-activating forms.

    Evidence Binding assays and heterologous DBD-fusion activation assays of chicken TEF-1A vs TEF-1B isoforms

    PMID:8106348

    Open questions at the time
    • Physiological relevance of isoform-specific activation not tested in vivo
    • Upstream splicing regulators not identified
  2. 1996 High

    Demonstrating that TEAD1 represses transcription by physically sequestering TBP away from TATA boxes revealed a cofactor-independent repression mechanism distinct from its activation function.

    Evidence GST pull-down of TBP, in vitro TBP-TATA competition assay, and co-transfection relief experiment in BeWo cells

    PMID:8621623

    Open questions at the time
    • Genome-wide extent of TBP-dependent repression unknown
    • Whether this mechanism operates in non-placental contexts untested
  3. 1997 High

    Cross-species rescue of Drosophila Scalloped mutants by human TEAD1 established deep evolutionary conservation of its DNA-binding and transcriptional activation functions.

    Evidence Transgenic Drosophila complementation of sd loss-of-function alleles

    PMID:9099715

    Open questions at the time
    • Whether mammalian cofactors (YAP/TAZ/VGLL) also complement Yki/Vg not tested
  4. 2002 High

    Identification of VGLL2 as a nuclear-translocating TEAD1 co-activator during myogenesis provided the first vertebrate Vestigial-like cofactor and linked TEAD1 to skeletal muscle differentiation.

    Evidence Mammalian two-hybrid, in vitro binding, reporter assays, and subcellular fractionation during C2C12 differentiation

    PMID:12376544

    Open questions at the time
    • In vivo requirement of VGLL2 for TEAD1-driven myogenesis not demonstrated
  5. 2004 High

    Mapping the SCRA-causing Y421H mutation to TEAD1's C-terminal domain linked a human retinal dystrophy to loss of the YAP-binding interface, providing the first disease gene assignment for TEAD1.

    Evidence Genome-wide linkage (LOD 18.9) in Icelandic SCRA families, sequencing, segregation in 81 patients/502 controls

    PMID:15016762

    Open questions at the time
    • Mechanism by which YAP-binding loss causes selective chorioretinal degeneration unknown
  6. 2005 High

    Discovery that TAZ physically engages TEAD1 on M-CAT DNA and activates TEAD1-dependent transcription established the second major Hippo effector–TEAD1 partnership and showed preferential TAZ binding to TEAD1 over TEAD4.

    Evidence GST pull-down, co-IP, mammalian two-hybrid, EMSA, and reporter assays

    PMID:15628970

    Open questions at the time
    • Structural basis for TEAD1-vs-TEAD4 selectivity of TAZ unresolved
  7. 2007 High

    Mutagenesis of the SCRA residue (Y410H in mouse) selectively ablated YAP/TAZ but not VGLL binding, defining two mechanistically separable cofactor interfaces on TEAD1.

    Evidence GST pull-down and reporter assays comparing wild-type and Y410H TEAD1 with YAP, TAZ, and VGLL1-3

    PMID:17689488

    Open questions at the time
    • Structural resolution of separate VGLL vs YAP/TAZ binding surfaces not provided
  8. 2011 High

    Identification of FoxO3a as a direct TEAD1 target in skeletal muscle connected TEAD1 to proteostasis and atrophy signaling beyond its known role in muscle-specific gene activation.

    Evidence ChIP-on-chip, ChIP-PCR, EMSA, luciferase reporter, and overexpression/knockdown in muscle cells

    PMID:21211055

    Open questions at the time
    • In vivo significance of TEAD1-FoxO3a axis for muscle atrophy not tested
  9. 2016 High

    Myofiber-specific TEAD1 overexpression revealed a non-cell-autonomous mechanism by which TEAD1-expressing fibers expand the satellite cell pool, linking TEAD1 to muscle regenerative capacity.

    Evidence Transgenic mouse overexpression, satellite cell quantification, injury regeneration, transplantation analysis

    PMID:27725085

    Open questions at the time
    • Identity of the secreted signal(s) mediating non-cell-autonomous satellite cell expansion unknown
  10. 2017 High

    Cardiomyocyte-specific Tead1 deletion causing lethal dilated cardiomyopathy via SERCA2a and Inhibitor-1 loss established TEAD1 as an essential regulator of cardiac calcium handling.

    Evidence Tamoxifen-inducible cardiac-specific KO mice, transcriptome analysis, validation in human iPS-cardiomyocytes

    PMID:28878117

    Open questions at the time
    • Whether TEAD1 cofactors YAP or VGLL mediate cardiac-specific target selection not determined
  11. 2018 High

    ChIP-validated TEAD1 occupancy at AQP4, EGFR, and CDH4 loci in glioblastoma, combined with CRISPR KO and rescue experiments, established TEAD1 as a driver of GBM cell migration through AQP4.

    Evidence ATAC-seq, ChIP-PCR, CRISPR-Cas9 KO, migration assays in vitro and in vivo, overexpression rescue

    PMID:30275445

    Open questions at the time
    • Whether AQP4-mediated migration requires YAP as cofactor not tested
  12. 2019 High

    VSMC-specific Tead1 KO embryonic lethality and identification of Pitx2c as a direct target—synergizing with myocardin—placed TEAD1 upstream of the core vascular smooth muscle differentiation cascade.

    Evidence Conditional KO mice (lethal E14.5), transcriptome analysis, rescue experiments

    PMID:31024075

    Open questions at the time
    • Whether TEAD1-Pitx2c axis operates in postnatal vascular remodeling not addressed
  13. 2021 High

    Genome-wide ChIP-seq in cardiomyocytes revealed that TEAD1 directly activates nuclear-encoded mitochondrial genes, and that its loss triggers necroptosis (rescuable by necrostatin-1), unifying the cardiac phenotype under a mitochondrial dysfunction mechanism.

    Evidence ChIP-seq, RNA-seq, mitochondrial functional assays, necrostatin-1 rescue in conditional KO mice

    PMID:33469230

    Open questions at the time
    • How TEAD1 coordinates mitochondrial gene regulation with SERCA2a/calcium targets unclear
  14. 2022 High

    Discovery of RBFOX2-mediated inclusion of TEAD1 exon 6 and its effect on YAP interaction strength provided the first upstream splicing code controlling TEAD1 transcriptional potency.

    Evidence Alternative splicing analysis, RBFOX2-GCAUG RNA binding, transcriptional and YAP interaction assays

    PMID:35699208

    Open questions at the time
    • Tissue-specific RBFOX2 regulation of TEAD1 splicing not mapped in vivo
  15. 2022 High

    Demonstration that TEAD1 represses target genes in pancreatic β cells by blocking RNA Pol II loading—independently of its YAP-binding pocket—established a second, cofactor-independent repression mode beyond TBP sequestration.

    Evidence Conditional β-cell KO, ChIP-seq, RNA-seq, Pol II occupancy assays in cancer cell lines

    PMID:36484096

    Open questions at the time
    • Structural basis for pocket-independent Pol II interference unknown
    • Whether this mechanism operates in cardiomyocytes untested
  16. 2023 High

    Identification of VGLL4 and MENIN as TEAD1 corepressors in β cells, repressing FZD7 and CCN2 independently of YAP/TAZ, revealed that TEAD1's role as a proliferation brake in endocrine cells uses a distinct cofactor repertoire.

    Evidence Split-GFP, yeast two-hybrid, conditional TEAD1/YAP/TAZ β-cell KO mice

    PMID:36662616

    Open questions at the time
    • Whether MENIN binding competes with or is simultaneous to VGLL4 not resolved
  17. 2024 High

    Characterization of TM7SF3/hnRNPU-controlled exclusion of TEAD1 exon 5 in hepatic stellate cells, with ASO-mediated splice correction reducing liver fibrosis in vivo, identified a second regulated splicing event and a therapeutic strategy.

    Evidence Conditional TM7SF3 KO, hnRNPU manipulation, ASO treatment, in vivo MASH model

    PMID:38670107

    Open questions at the time
    • Whether exon 5 and exon 6 splicing events interact or are independently regulated unknown
  18. 2024 High

    SUMOylation at K173 was shown to stabilize TEAD1 protein, promote nuclear retention, and enhance YAP interaction, with deSUMOylation exacerbating cardiac hypertrophy in vivo, adding a post-translational layer of TEAD1 regulation.

    Evidence K173 mutagenesis, SUMOylation assay, co-IP, DNA-binding assay, AAV9 delivery in mouse hypertrophy model

    PMID:38225750

    Open questions at the time
    • Signal-dependent regulation of SENP1/SUMO1 balance at TEAD1 unknown
    • Whether SUMOylation affects VGLL4/MENIN co-repressor binding untested
  19. 2024 High

    Schwann cell-specific TEAD1 KO abolishing myelination and Remak bundle formation, via Krox20/Egr2 and cholesterol biosynthesis gene regulation, extended TEAD1's essential roles to the peripheral nervous system.

    Evidence Conditional and inducible SC-specific KO mice, electron microscopy, gene expression analysis, nerve function assays

    PMID:38456457

    Open questions at the time
    • Whether TEAD1 acts with YAP or VGLL cofactors in Schwann cells not determined
  20. 2024 High

    Identification of BRD4 as a TEAD1 interactor driving Wnt4-dependent cardiac fibroblast activation, with both genetic KO and pharmacological TEAD1 inhibition (VT103) rescuing cardiac fibrosis, provided a druggable mechanism.

    Evidence Co-IP/MS, ChIP-seq, luciferase, conditional KO, VT103 treatment in TAC model

    PMID:38374140

    Open questions at the time
    • Whether BRD4-TEAD1 interaction is direct or bridged by chromatin context not resolved
    • Selectivity of VT103 for TEAD1 vs other TEAD family members unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • Major unresolved questions include the structural basis for TEAD1's dual activation/repression switching, how tissue-specific cofactor selection (YAP/TAZ vs VGLL vs VGLL4/MENIN) is determined, and the interplay between alternative splicing (exon 5 vs exon 6) and post-translational modifications (SUMOylation, palmitoylation) in controlling TEAD1 output in different cell types.
  • No high-resolution structure of full-length TEAD1 with cofactor switching intermediates
  • Integrated model of splicing and PTM regulation across tissues absent
  • Mechanistic basis for non-cell-autonomous signaling from TEAD1-expressing myofibers remains unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 10 GO:0003677 DNA binding 5
Localization
GO:0005634 nucleus 3
Pathway
R-HSA-74160 Gene expression (Transcription) 10 R-HSA-162582 Signal Transduction 7 R-HSA-1266738 Developmental Biology 4 R-HSA-5357801 Programmed Cell Death 2 R-HSA-397014 Muscle contraction 1
Partners
BRD4MEN1VGLL1VGLL2VGLL3VGLL4WWTR1YAP1
Complex memberships
TAZ-TEAD1TEAD1-BRD4YAP-TEAD1

Evidence

Reading pass · 36 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 TAZ (transcriptional co-activator with PDZ-binding motif) interacts with TEAD1 (TEF-1) both in vitro and in vivo; GST pull-down assays showed TAZ interacts with TEAD1 bound to MCAT DNA, and TAZ can activate MCAT-dependent reporter promoters through endogenous TEAD1; TAZ interacts more efficiently with TEAD1 than with RTEF-1 (TEAD4), indicating differential cofactor association among family members. GST pull-down, co-immunoprecipitation, mammalian two-hybrid, EMSA, reporter assay The Biochemical journal High 15628970
2002 Mammalian Vestigial-like 2 (Vgl-2) interacts with TEAD1 (TEF-1) in vitro and in vivo via a conserved TEF-1 interaction domain; during skeletal muscle differentiation, Vgl-2 protein translocates from cytoplasm to nucleus and co-activates TEAD1-dependent promoters alongside MEF2. Mammalian two-hybrid, in vitro binding, co-expression reporter assay, subcellular fractionation The Journal of biological chemistry High 12376544
1994 Chicken TEF-1 (TEAD1) isoforms TEF-1A and TEF-1B both bind M-CAT elements with high affinity and sequence specificity; the C-terminal portion of TEF-1B (containing a unique 13-amino acid exon) can activate transcription when fused to a heterologous DNA-binding domain, whereas the equivalent domain of TEF-1A cannot, demonstrating isoform-specific transcriptional activation activity. Binding assays, transcriptional activation assay with heterologous DBD fusion, isoform cloning The Journal of biological chemistry High 8106348
2004 A missense mutation Y421H in TEAD1 is the causative allele for Sveinsson's chorioretinal atrophy (SCRA); the mutation resides in a conserved C-terminal region proposed to be the YAP65 binding site; TEAD1 and YAP65 are both expressed in human retina by RT-PCR. Genome-wide linkage analysis, sequencing, RT-PCR expression analysis Human molecular genetics High 15016762
2007 The SCRA-associated mutation Y410H (equivalent to human Y421H) in mouse Tead1 specifically abolishes interaction with co-factors YAP and TAZ but not with Vgl-1, -2, or -3; direct interaction between Tead1 and YAP or TAZ is lost due to this mutation as shown by GST pull-down; the Y410H mutation also abolishes TEAD1 transcriptional activity under YAP or TAZ co-expression, establishing that Tyr410 is essential for YAP/TAZ binding. Mammalian two-hybrid, GST pull-down, site-directed mutagenesis, reporter assay Biochemical and biophysical research communications High 17689488
1996 TEAD1 (TEF-1) represses transcription in BeWo choriocarcinoma cells through direct physical interaction with the TATA-binding protein (TBP); GST-TEF-1 fusion peptides retained in vitro-generated TBP, with the proline-rich domain essential for TBP binding; TEF-1 inhibited TBP binding to the TATA motif in vitro; co-expression of TBP with TEF-1 relieved TEF-1-mediated transrepression in vivo. GST pull-down, in vitro TBP binding/competition assay, co-transfection reporter assay, antisense oligonucleotide The Journal of biological chemistry High 8621623
1997 Human TEAD1 (TEF-1) can functionally substitute for Drosophila Scalloped (TEF-1 homolog) in vivo, rescuing wingblade defects and lethality of loss-of-function alleles and promoting sd gene regulation in imaginal wing discs, establishing functional conservation of the DNA-binding and activation domains. Transgenic Drosophila rescue of loss-of-function alleles, enhancer-trap reporter assay The Journal of biological chemistry High 9099715
2017 Adult cardiomyocyte-specific Tead1 deletion causes lethal acute-onset dilated cardiomyopathy with impaired excitation-contraction coupling; Tead1 directly activates SERCA2a and Inhibitor-1 (I-1) transcription, and its loss leads to decreased SERCA2a and I-1 protein, increased PP1 activity, accumulation of dephosphorylated phospholamban, and decreased SERCA2a activity. Tamoxifen-inducible cardiac-specific knockout mice, transcriptome analysis, ChIP (implied by direct target characterization), functional cardiac assays, human iPS-derived cardiomyocyte validation JCI insight High 28878117
2019 TEAD1 is essential for vascular smooth muscle cell (VSMC) differentiation and proliferation; VSMC-specific Tead1 knockout mice exhibit embryonic lethality (E14.5) with hypoplastic vascular walls; Tead1 deletion downregulates muscle contractile genes and key transcription factors including Pitx2c and myocardin; Pitx2c is identified as a novel direct transcriptional target of TEAD1, and PITX2c synergizes with myocardin (via direct interaction) to rescue TEAD1-dependent VSMC differentiation defects. Conditional knockout mice, whole-transcriptome analysis, in vitro rescue experiments, ChIP (implied by direct target analysis) Cell death and differentiation High 31024075
2021 Tead1 deletion in adult cardiomyocytes activates necroptosis (not apoptosis) and causes dilated cardiomyopathy; genome-wide ChIP-seq and transcriptomics revealed Tead1 directly activates nuclear DNA-encoded mitochondrial genes required for electron transfer complex assembly and ATP production; Tead1 loss increases mitochondrial ROS, disrupts mitochondrial structure, and reduces complex I-IV oxygen consumption; blocking necroptosis with necrostatin-1 rescues Tead1 deletion-induced heart failure. Conditional and ubiquitous Tead1 KO mice, ChIP-seq, RNA-seq, mitochondrial functional assays, necrostatin-1 rescue Cell death and differentiation High 33469230
2018 In glioblastoma, TEAD1 directly occupies chromatin at the AQP4, EGFR, and CDH4 loci (validated by ChIP-PCR); CRISPR-Cas9 knockout of TEAD1 robustly diminishes glioblastoma migration in vitro and in vivo, with consistent downregulation of AQP4; TEAD1 overexpression restores AQP4 expression, and overexpression of either TEAD1 or AQP4 rescues migratory deficits in TEAD1-KO cells, establishing a TEAD1–AQP4 regulatory axis for GBM migration. ATAC-seq, ChIP-PCR, CRISPR-Cas9 KO, migration assays in vitro and in vivo, overexpression rescue Nature communications High 30275445
2018 YAP1-TEAD1 signaling controls mitochondrial biogenesis and angiogenesis in endothelial cells through PGC1α; TEAD1 knockdown decreases PGC1α expression and suppresses mitochondrial biogenesis, glycolysis, and oxygen consumption; a YAP1 mutant (S94A) that cannot bind TEAD1 fails to upregulate PGC1α or induce mitochondrial biogenesis, while the TEAD1-binding mutant (S127A) does; PGC1α knockdown inhibits YAP1-induced angiogenesis. siRNA knockdown, YAP1 domain mutants (S127A vs S94A), mitochondrial biogenesis assays, in vitro sprouting, in vivo fibrin gel vascular morphogenesis Microvascular research High 29680477
2019 VGLL3 binds TEAD1, TEAD3, and TEAD4 in myoblasts and/or myotubes (identified by interaction proteomics); unlike YAP and TAZ, VGLL3 does not interact with components of the Hippo kinase cascade; VGLL3 overexpression reduces Hippo negative-feedback loop activity and promotes myogenic differentiation, while siRNA-mediated Vgll3 knockdown suppresses myoblast proliferation. Interaction proteomics (pull-down/MS), siRNA knockdown, overexpression, gene expression profiling Journal of cell science High 31138678
2011 TEAD1 directly regulates FoxO3a transcription in skeletal muscle by binding to an M-CAT element in the foxo3a promoter, demonstrated by ChIP-on-chip, independent ChIP-PCR, EMSA, and luciferase reporter assay; overexpression and inhibition experiments confirm that foxo3a is positively regulated by TEAD1. ChIP-on-chip, ChIP-PCR, EMSA, luciferase reporter assay, overexpression/knockdown BMC molecular biology High 21211055
2015 TEAD1 knockdown in prostate cell lines (PC3 and RWPE1) leads to decreased cell growth and disrupted acinar formation in 3D culture, establishing a cell-autonomous role for TEAD1 in prostate epithelial cell proliferation and glandular architecture. siRNA knockdown, cell growth assay, 3D culture acinar formation assay British journal of cancer Medium 19002168
2016 Myofiber-specific TEAD1 overexpression in transgenic mice causes dramatic hyperplasia of muscle satellite cells (SCs) without affecting muscle size; hyperplastic SCs are normally quiescent, accelerate regeneration, and are accumulated non-cell-autonomously via signals from TEAD1-expressing myofibers; TEAD1 transgene also ameliorates dystrophic muscle pathology. Transgenic mouse overexpression, satellite cell quantification, injury-induced regeneration assays, transplantation/non-cell-autonomous signal analysis eLife High 27725085
2015 TEAD1 acts as a direct transcriptional activator of the HPV early promoter and cooperates with VGLL1 cofactor to drive HPV early gene expression; 11 TEAD1 target sites were identified in the HPV16 long control region (LCR) by in vitro DNA pulldown, 8 of which activate the early promoter in luciferase assays; VGLL1 binds to the LCR via its interaction with TEAD1 in vitro and in vivo; knockdown of VGLL1 and/or TEAD1 decreases viral early gene expression. In vitro DNA pulldown, luciferase reporter assay, ChIP, siRNA knockdown Journal of virology High 32132238
2016 TEAD1 regulates C-MYC and GLUT1 expression in human leukemia cells through the MST1-YAP1-TEAD1 axis; YAP1 positively regulates C-MYC mRNA in complex with TEAD1; specific depletion of TEAD1 decreases lactate production; TEAD-binding motifs in C-MYC and GLUT1 promoters were identified bioinformatically, supporting direct transcriptional regulation. RNAi knockdown, lactate production assay, bioinformatics promoter analysis, shikonin-mediated MST1 activation Experimental cell research Medium 27793648
2021 The YAP/TEAD1 complex acts as a default repressor of cardiac Toll-like receptor genes; TEAD1 directly binds genomic regions adjacent to Tlr1-7 and Tlr9 (by ChIP); in vitro luciferase assays show YAP/TEAD1 repression of Tlr4 requires a conserved TEAD1 binding motif near the Tlr4 TSS; cardiomyocyte-specific YAP depletion in vivo increases expression of most examined TLR genes and activates pro-inflammatory cytokine synthesis. ChIP, luciferase reporter assay with TEAD1 binding motif mutation, cardiomyocyte-specific YAP KO mouse, cytokine profiling International journal of molecular sciences High 34206257
2022 RBFOX2 promotes inclusion of TEAD1 exon 6 via binding to a conserved GCAUG element in the downstream intron; the full-length TEAD1 isoform (with exon 6) has greater transcriptional activity and oncogenic properties than TEAD1ΔE6, with the difference in transcription related to YAP interaction; expression of YAP-TEAD target genes negatively correlates with TEAD1ΔE6 expression. Alternative splicing analysis, RNA binding assay (RBFOX2-GCAUG), transcriptional activity assays, YAP interaction assays, bioinformatics Nucleic acids research High 35699208
2024 TM7SF3 deletion promotes alternative splicing of TEAD1 by inhibiting the splicing factor hnRNPU, resulting in exclusion of inhibitory exon 5 and generation of a more transcriptionally active TEAD1 isoform that triggers hepatic stellate cell (HSC) activation and liver fibrosis; inhibiting TEAD1 alternative splicing with a specific antisense oligomer (ASO) deactivates HSCs in vitro and reduces MASH diet-induced liver fibrosis in vivo. Conditional TM7SF3 KO, alternative splicing analysis, hnRNPU manipulation, ASO treatment, in vitro HSC activation assay, in vivo MASH model Cell metabolism High 38670107
2022 TEAD1 exerts a pocket region-independent direct transcriptional repression mechanism by interfering with RNA Polymerase II binding to target promoters; conditional pancreatic β-cell TEAD1 knockout leads to cell-autonomous increase in β-cell proliferation independently of YAP/TAZ; genome-wide ChIP-seq and transcriptomics identified direct TEAD1-repressed target genes in a motif-dependent, orientation-independent manner. Conditional β-cell KO mice, ChIP-seq, RNA-seq, cancer cell line overexpression, POLII binding assay Nucleic acids research High 36484096
2023 VGLL4 and MENIN function as TEAD1 corepressors in pancreatic β cells; using split-GFP and yeast two-hybrid platforms, VGLL4 and MENIN were shown to bind TEAD1 and repress expression of target genes FZD7 and CCN2, thereby inhibiting β cell proliferation; β cell-specific deletion of TEAD1 (but not YAP/TAZ) increases β cell proliferation, confirming a YAP/TAZ-independent repressive mechanism. Split-GFP system, yeast two-hybrid, conditional β-cell KO mice (TEAD1, YAP, TAZ), gene expression analysis Cell reports High 36662616
2021 Tead1 induces cardiac fibroblast-to-cardiomyocyte reprogramming; Tead1 overexpression (substituting for TBX5 in GMT cocktail) nearly triples cardiomyocyte marker cTnT expression in mouse embryonic and adult rat fibroblasts, enables sarcomere organization and contractility (beating) in reprogrammed cells; mechanistically, GMTd increases H3K4me3 marks at promoters of cardio-differentiation and mitochondrial biogenesis genes. Fibroblast reprogramming assay, flow cytometry for cTnT, sarcomere organization imaging, contractility measurement, ChIP for H3K4me3 Journal of the American Heart Association Medium 34889103
2013 TEAD1 positively activates transcription of the NAIP (neuronal apoptosis inhibitory protein) gene through an intronic regulatory region; this activation requires interaction with the endogenous YAP cofactor, as demonstrated by reporter assays and co-expression experiments. Reporter assay, co-expression with YAP, intronic regulatory region mapping FEBS letters Medium 23994529
2024 TEAD1 promotes cardiac fibroblast-to-myofibroblast transition through a BRD4/Wnt4 signaling pathway; co-IP combined with mass spectrometry identified BRD4 as a TEAD1 interactor; ChIP-seq and luciferase assays showed TEAD1 and BRD4 bind and activate the Wnt4 promoter; genetic Wnt4 knockdown inhibited the pro-transformation phenotype in cardiac fibroblasts with TEAD1 overexpression; CF/myofibroblast-specific TEAD1 KO and TEAD1 inhibitor VT103 both ameliorated TAC-induced cardiac remodeling in vivo. Co-IP with mass spectrometry, ChIP-seq, luciferase assay, RNA-seq, conditional KO mice, pharmacological inhibition (VT103), echocardiography Signal transduction and targeted therapy High 38374140
2024 SUMOylation of TEAD1 at lysine 173 by SUMO1 (deSUMOylation regulated by SENP1) affects TEAD1 protein stability, nuclear localization, and DNA-binding ability, and enhances interaction between TEAD1 and YAP1; deSUMOylation of TEAD1 (KR mutant) exacerbates cardiomyocyte hypertrophy in vitro and in a mouse cardiac hypertrophy model (AAV9 delivery). Site-directed mutagenesis of K173, SUMOylation assay, nuclear localization analysis, co-IP (TEAD1-YAP1), DNA-binding assay, AAV9 in vivo delivery, echocardiography Advanced science High 38225750
2024 TEAD1 is essential for Schwann cell myelination; conditional TEAD1 KO abolishes SC myelination development and regeneration; TEAD1 promotes myelination by regulating SC proliferation, enabling Krox20/Egr2 to upregulate myelin proteins, and upregulating cholesterol biosynthetic enzymes FDPS and IDI1; non-myelinating SCs uniquely require TEAD1 to enwrap nociceptive axons in Remak bundles. Conditional and inducible Schwann cell-specific KO mice, electron microscopy, gene expression analysis, functional nerve assessments eLife High 38456457
2023 TEAD1 and YAP1 co-localize in trophectoderm and primitive endoderm precursor cells during human preimplantation development, suggesting roles in both first (ICM vs TE) and second (EPI vs PrE) lineage segregation events; TEAD1 displays a distinct spatial pattern coinciding with YAP1/GATA3 co-localization in outer/TE cells, with lower levels in ICM cells. Immunofluorescence/confocal imaging of human preimplantation embryos, co-localization analysis Human reproduction Medium 37295962
2024 TEAD1 interacts with PGC-1α (peroxisomal proliferator-γ coactivator-1α) to promote mitochondrial function in proximal tubule cells; proximal tubule-specific TEAD1 KO enhances necroptosis, inflammatory response, and mitochondrial dysfunction (increased ROS, reduced ATP) in cisplatin-induced acute kidney injury. Proximal tubule conditional KO mice, co-immunoprecipitation (TEAD1-PGC1α), mitochondrial bioenergetics assays, necroptosis pathway analysis International journal of biological sciences Medium 39781453
2020 YAP-TEAD1 complex targets key genes encoding proteins involved in cytoskeleton dynamics and focal adhesion stability in human pluripotent stem cells (PSCs); inactivation of YAP-TEAD1 is required for adjustment of PSC mechanical properties during germ layer specification; aberrant YAP-TEAD1 activation alters PSC potency by inhibiting cytoskeleton dynamics. Tankyrase inhibitor to modulate AMOT/YAP, gene expression analysis, mechanobiology assays on substrates of defined stiffness Cell death and differentiation Medium 33116297
2021 TEAD1 knockdown in mouse skin fibroblasts attenuates SA-β-Gal activity and partially alters the replicative senescence-associated transcriptome, identifying TEAD1 as a transcriptional regulator of the senescence program. siRNA knockdown, ATAC-seq/RRBS/RNA-seq multi-omics, SA-β-Gal activity assay Protein & cell Medium 35023014
2021 RGS12 negatively regulates the transcriptional activity of the YAP/TEAD1 complex through its PDZ domain to inhibit expression of the osteosarcoma marker Ezrin; RGS12 knockdown upregulates Ezrin via GNA12/13-RhoA-YAP pathway and TEAD1 complex activity. siRNA knockdown, PDZ domain peptide competition, luciferase reporter assay, orthotopic xenograft mouse model Oncogene Medium 33686240
2024 TEAD1 directly regulates ITGA1 and ITGA2 integrin gene expression in prostate cancer cells; TEAD1 loss phenocopies dual ITGA1/ITGA2 loss by inducing EMT via enhanced TGFβ1 secretion and nuclear YAP1 targeting in vitro and in vivo. Genome-wide co-expression analysis, TEAD1 loss-of-function, in vitro EMT assays, in vivo tumor model Advanced science Medium 38169150
2015 TEAD1 positively feedback regulates miR-222 transcription in gastric cancer cells by physically binding to the miR-222 promoter (demonstrated by ChIP assay); miR-222 in turn suppresses VGLL4 (a TEAD1 co-repressor), maintaining over-activated YAP-TEAD1 signaling in a regulatory loop. ChIP assay for TEAD1 at miR-222 promoter, siRNA knockdown, luciferase reporter assay American journal of cancer research Medium 26045994
2024 Endothelial YAP/TEAD1-CXCL17 signaling recruits myeloid-derived suppressor cells (MDSCs) during liver ischemia-reperfusion injury; hypoxia-reoxygenation stimulation activates the YAP/TEAD1 complex in hepatic endothelial cells to promote CXCL17 transcription, and CXCL17 recruits MDSCs via GPR35. Single-cell RNA-seq, bulk RNA-seq, in vivo YAP/TEAD1 modulation, adoptive MDSC transfer, mechanistic in vitro experiments Hepatology Medium 38407233

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2020 Systemic amyloidosis from A (AA) to T (ATTR): a review. Journal of internal medicine 221 32929754
2014 AA amyloidosis: pathogenesis and targeted therapy. Annual review of pathology 202 25387054
2005 The transcriptional co-activator TAZ interacts differentially with transcriptional enhancer factor-1 (TEF-1) family members. The Biochemical journal 180 15628970
2002 Pathology, diagnosis and pathogenesis of AA amyloidosis. Virchows Archiv : an international journal of pathology 169 11964039
2018 Secondary, AA, Amyloidosis. Rheumatic diseases clinics of North America 144 30274625
2008 GLUE-IT and PEDEL-AA: new programmes for analyzing protein diversity in randomized libraries. Nucleic acids research 141 18442989
2002 Mammalian vestigial-like 2, a cofactor of TEF-1 and MEF2 transcription factors that promotes skeletal muscle differentiation. The Journal of biological chemistry 139 12376544
1988 Cerebral arteriovenous malformations (C. AVM) and associated arterial aneurysms (AA). Analysis of 101 C. AVM cases, with 37 AA in 23 patients. Acta neurochirurgica 135 3293363
2004 Epidemiological and sequence differences between two subtypes (Ae and Aa) of hepatitis B virus genotype A. The Journal of general virology 118 15039524
2004 A novel TEAD1 mutation is the causative allele in Sveinsson's chorioretinal atrophy (helicoid peripapillary chorioretinal degeneration). Human molecular genetics 113 15016762
2007 Ribosome kinetics and aa-tRNA competition determine rate and fidelity of peptide synthesis. Computational biology and chemistry 111 17897886
2014 Rapid diversification of five Oryza AA genomes associated with rice adaptation. Proceedings of the National Academy of Sciences of the United States of America 102 25368197
1994 Muscle-enriched TEF-1 isoforms bind M-CAT elements from muscle-specific promoters and differentially activate transcription. The Journal of biological chemistry 99 8106348
2016 Endogenous GABAA receptor activity suppresses glioma growth. Oncogene 84 27375015
2008 TEAD1 and c-Cbl are novel prostate basal cell markers that correlate with poor clinical outcome in prostate cancer. British journal of cancer 80 19002168
2018 Analysis of chromatin accessibility uncovers TEAD1 as a regulator of migration in human glioblastoma. Nature communications 75 30275445
2007 A Sveinsson's chorioretinal atrophy-associated missense mutation in mouse Tead1 affects its interaction with the co-factors YAP and TAZ. Biochemical and biophysical research communications 75 17689488
2017 TEAD1/4 exerts oncogenic role and is negatively regulated by miR-4269 in gastric tumorigenesis. Oncogene 73 28759040
2006 Stability of DNA duplexes containing GG, CC, AA, and TT mismatches. Biochemistry 71 16939208
2013 Transmission of systemic AA amyloidosis in animals. Veterinary pathology 68 24280941
2009 Serum amyloid A and protein AA: molecular mechanisms of a transmissible amyloidosis. FEBS letters 65 19393650
2019 VGLL3 operates via TEAD1, TEAD3 and TEAD4 to influence myogenesis in skeletal muscle. Journal of cell science 63 31138678
2017 Tead1 is required for maintaining adult cardiomyocyte function, and its loss results in lethal dilated cardiomyopathy. JCI insight 58 28878117
2019 Development and Testing of the OPLS-AA/M Force Field for RNA. Journal of chemical theory and computation 54 30807148
1999 Transgenic mouse model of AA amyloidosis. The American journal of pathology 54 10233864
2020 Germacrene A-A Central Intermediate in Sesquiterpene Biosynthesis. Chemistry (Weinheim an der Bergstrasse, Germany) 52 32442350
2015 Genetic variants in Hippo pathway genes YAP1, TEAD1 and TEAD4 are associated with melanoma-specific survival. International journal of cancer 51 25628125
2019 Transcription factor TEAD1 is essential for vascular development by promoting vascular smooth muscle differentiation. Cell death and differentiation 48 31024075
2016 An evolutionary, structural and functional overview of the mammalian TEAD1 and TEAD2 transcription factors. Gene 48 27421669
2021 TEAD1 protects against necroptosis in postmitotic cardiomyocytes through regulation of nuclear DNA-encoded mitochondrial genes. Cell death and differentiation 46 33469230
2020 YAP-TEAD1 control of cytoskeleton dynamics and intracellular tension guides human pluripotent stem cell mesoderm specification. Cell death and differentiation 46 33116297
2018 YAP1-TEAD1 signaling controls angiogenesis and mitochondrial biogenesis through PGC1α. Microvascular research 45 29680477
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2020 Episignatures Stratifying Helsmoortel-Van Der Aa Syndrome Show Modest Correlation with Phenotype. American journal of human genetics 42 32758449
2017 MiR-590-3p suppresses hepatocellular carcinoma growth by targeting TEAD1. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 42 28349829
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1987 Cell volume regulation in hemoglobin CC and AA erythrocytes. The American journal of physiology 37 3826359
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2010 Negative affect, relapse, and Alcoholics Anonymous (AA): does AA work by reducing anger? Journal of studies on alcohol and drugs 36 20409438
2018 AA amyloidosis - Benefits and prospects of IL-6 inhibitors. Modern rheumatology 35 30132351
1996 TEF-1 transrepression in BeWo cells is mediated through interactions with the TATA-binding protein, TBP. The Journal of biological chemistry 35 8621623
2024 TEA domain transcription factor 1(TEAD1) induces cardiac fibroblasts cells remodeling through BRD4/Wnt4 pathway. Signal transduction and targeted therapy 34 38374140
2022 Unveiling E2F4, TEAD1 and AP-1 as regulatory transcription factors of the replicative senescence program by multi-omics analysis. Protein & cell 34 35023014
2020 LncRNA Kcnq1ot1 renders cardiomyocytes apoptosis in acute myocardial infarction model by up-regulating Tead1. Life sciences 34 32422306
1997 The human transcription enhancer factor-1, TEF-1, can substitute for Drosophila scalloped during wingblade development. The Journal of biological chemistry 34 9099715
2019 Long non‑coding RNA LINC00473/miR‑195‑5p promotes glioma progression via YAP1‑TEAD1‑Hippo signaling. International journal of oncology 33 31894297
2015 Predictors of AA amyloidosis in familial Mediterranean fever. Rheumatology international 32 25586652
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2023 Lineage segregation in human pre-implantation embryos is specified by YAP1 and TEAD1. Human reproduction (Oxford, England) 30 37295962
2021 Hippo Pathway Effector Tead1 Induces Cardiac Fibroblast to Cardiomyocyte Reprogramming. Journal of the American Heart Association 30 34889103
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2011 TEAD1-dependent expression of the FoxO3a gene in mouse skeletal muscle. BMC molecular biology 28 21211055
2022 Development of Lipo-γ-AA Peptides as Potent Antifungal Agents. Journal of medicinal chemistry 26 35637173
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2021 RGS12 is a novel tumor suppressor in osteosarcoma that inhibits YAP-TEAD1-Ezrin signaling. Oncogene 25 33686240
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2021 YAP/TEAD1 Complex Is a Default Repressor of Cardiac Toll-Like Receptor Genes. International journal of molecular sciences 23 34206257
2015 A De Novo Mutation in TEAD1 Causes Non-X-Linked Aicardi Syndrome. Investigative ophthalmology & visual science 23 26091538
2000 PolyHEMA and polyHEMA-poly(MMA-co-AA) as substrates for culturing Vero cells. Journal of materials science. Materials in medicine 23 15348383
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2024 Endothelial YAP/TEAD1-CXCL17 signaling recruits myeloid-derived suppressor cells against liver ischemia-reperfusion injury. Hepatology (Baltimore, Md.) 21 38407233
2020 The metalloproteinase Papp-aa controls epithelial cell quiescence-proliferation transition. eLife 20 32293560
2021 Two Distinct Faces of Vitamin C: AA vs. DHA. Antioxidants (Basel, Switzerland) 19 33535710
2016 Myofiber-specific TEAD1 overexpression drives satellite cell hyperplasia and counters pathological effects of dystrophin deficiency. eLife 19 27725085
2000 Tumor cell splice variants of the transcription factor TEF-1 induced by SV40 T-antigen transformation. Biochimica et biophysica acta 19 11118619
2016 Vitamin D supplementation reduces some AT1-AA-induced downstream targets implicated in preeclampsia including hypertension. American journal of physiology. Regulatory, integrative and comparative physiology 18 27903510
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2013 An update on adding docosahexaenoic acid (DHA) and arachidonic acid (AA) to baby formula. Food & function 18 24150114
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2020 The Transcriptional Cofactor VGLL1 Drives Transcription of Human Papillomavirus Early Genes via TEAD1. Journal of virology 17 32132238
1994 A TEF-1 binding motif that interacts with a placental protein is important for the transcriptional activity of the hCS-B enhancer. DNA and cell biology 17 7945936
2020 Arsenic trioxide-induced upregulation of miR-1294 suppresses tumor growth in hepatocellular carcinoma by targeting TEAD1 and PIM1. Cancer biomarkers : section A of Disease markers 16 32280078
1994 Prevalence and distribution of bacteriophage phi Aa DNA in strains of Actinobacillus actinomycetemcomitans. FEMS microbiology letters 16 8050714
2024 Dampened Regulatory Circuitry of TEAD1/ITGA1/ITGA2 Promotes TGFβ1 Signaling to Orchestrate Prostate Cancer Progression. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 15 38169150
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2023 VGLL4 and MENIN function as TEAD1 corepressors to block pancreatic β cell proliferation. Cell reports 14 36662616
2022 CircSLC8A1 Exacerbates Hypoxia-Induced Myocardial Injury via Interacting with MiR-214-5p to Upregulate TEAD1 Expression. International heart journal 14 35650159
2020 Circular RNA Gprc5a Promotes HCC Progression by Activating YAP1/TEAD1 Signalling Pathway by Sponging miR-1283. OncoTargets and therapy 14 32547082
2018 Chloroplast phylogeography of AA genome rice species. Molecular phylogenetics and evolution 14 29753711
2008 Lovastatin inhibits formation of AA amyloid. Journal of leukocyte biology 14 18285405
2024 SUMOylation of TEAD1 Modulates the Mechanism of Pathological Cardiac Hypertrophy. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 13 38225750
2023 Matrix Stiffness Activating YAP/TEAD1-Cyclin B1 in Nucleus Pulposus Cells Promotes Intervertebral Disc Degeneration. Aging and disease 13 37196128
2021 LncRNA ASB16-AS1 drives proliferation, migration, and invasion of colorectal cancer cells through regulating miR-185-5p/TEAD1 axis. Cell cycle (Georgetown, Tex.) 13 34870557
2008 PDGF receptor-{beta} modulates metanephric mesenchyme chemotaxis induced by PDGF AA. American journal of physiology. Renal physiology 13 19019919
2025 TEAD1 Prevents Necroptosis and Inflammation in Cisplatin-Induced Acute Kidney Injury Through Maintaining Mitochondrial Function. International journal of biological sciences 12 39781453
2017 Clinical outcomes and survival in AA amyloidosis patients. Revista brasileira de reumatologia 12 29173691
2013 Interaction with the Yes-associated protein (YAP) allows TEAD1 to positively regulate NAIP expression. FEBS letters 12 23994529
2012 Biological responses to PDGF-AA versus PDGF-CC in renal fibroblasts. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 12 23229927
2023 LncRNA AP000695.2 promotes glycolysis of lung adenocarcinoma via the miR-335-3p/TEAD1 axis. Acta biochimica et biophysica Sinica 11 37723874