Affinage

Showing TEAD2 — ETF is a alias.

TEAD2

Transcriptional enhancer factor TEF-4 · UniProt Q15562

Length
447 aa
Mass
49.2 kDa
Annotated
2026-06-10
58 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TEAD2 (originally identified as the transcription factor ETF) is a TEA/ATTS-domain DNA-binding transcription factor that partners with Hippo-pathway co-activators to control proliferation, embryonic development, stem cell state, and tumorigenesis (PMID:9502435, PMID:18332127, PMID:38605224). Its DNA-binding TEA domain recognizes M-CAT/GT-IIC elements and preferentially activates GC-rich, TATA-less promoters (PMID:9502435, PMID:2768275), while a separate immunoglobulin-like YAP-binding domain presents an extensive conserved surface that docks the natively unfolded TEAD-binding region of YAP (PMID:20368466). Because TEAD2 relies on recruited co-activators, transcriptional output is set by YAP/TAZ engagement: in mouse ES cells a Yes-kinase–YAP–TEAD2 axis drives Oct-3/4 and Nanog promoter activity to sustain self-renewal (PMID:21385842), and TEAD1/TEAD2 use YAP as their major coactivator in vivo, with double-knockout embryos dying at E9.5 with growth failure, loss of notochord maintenance, and reduced proliferation (PMID:18332127). In development TEAD2 activates lineage enhancers, directly binding a Pax3 neural-crest enhancer and the Fgfr4 promoter through an M-CAT motif (PMID:14736747, PMID:16267055), and is independently required for neural tube closure (PMID:17868131). In ES cells TEAD2 reorganizes the genome, gaining chromatin occupancy in the ground state and mediating enhancer–promoter looping at 2i-specific loci independently of CTCF and YY1 (PMID:38605224). When aberrantly activated TEAD2 is oncogenic: it cooperates with TAZ to upregulate ANLN and KIF23 in hepatocellular carcinoma (PMID:36894036), activates the TAK1 promoter to drive sorafenib resistance (PMID:39106149), represses acetyl-CoA biosynthesis pathways in HCC (PMID:36400009), and establishes a proangiogenic enhancer landscape via CD109 in basal-like pancreatic cancer (PMID:36907523).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1989 High

    Established the founding biochemical activity of TEAD2/ETF as a transcription factor with a defined promoter preference, answering what kind of promoters it acts on.

    Evidence In vitro transcription and gel-shift assays with TATA-box substitution across promoter variants

    PMID:2768275

    Open questions at the time
    • Did not identify the co-activator requirement
    • Physiological target genes not defined
  2. 1998 Medium

    Cloned full-length ETF/TEAD2 and assigned its TEA/ATTS DNA-binding domain and a transcriptional activation capacity, defining the protein architecture.

    Evidence cDNA cloning, gel mobility shift on M-CAT/GT-IIC elements, GAL4-fusion activation assay

    PMID:9502435

    Open questions at the time
    • GAL4-fusion activation does not establish intrinsic activation in native context
    • Co-activator dependence not addressed
  3. 2004 High

    Connected TEAD2 to a specific developmental enhancer, showing it directly activates Pax3 in the dorsal neural tube and identifying YAP65 as a co-expressed partner.

    Evidence Transgenic mouse reporters, binding-site mutagenesis, dominant-negative Tead2-Engrailed fusion

    PMID:14736747

    Open questions at the time
    • Direct biochemical TEAD2-YAP interaction not shown here
    • Whether YAP is the functional coactivator at this enhancer untested
  4. 2005 High

    Placed TEAD2 in a defined transcriptional cascade by showing it activates Fgfr4 through an M-CAT motif while being itself a MyoD target, linking it to muscle regeneration.

    Evidence ChIP, promoter reporters with M-CAT mutagenesis, Fgfr4-null regeneration phenotype

    PMID:16267055

    Open questions at the time
    • Co-activator at the Fgfr4 promoter not identified
    • TEAD2-specific loss-of-function in muscle not tested
  5. 2007 Medium

    Revealed a developmental role distinct from its enhancer targets, showing Tead2 loss causes neural tube closure defects independent of Pax3 regulation.

    Evidence Mouse knockout phenotyping with folic acid and pifithrin-alpha rescue

    PMID:17868131

    Open questions at the time
    • Molecular pathway for exencephaly not defined
    • Maternal genetic contribution mechanism unresolved
  6. 2008 High

    Demonstrated in vivo that TEAD1 and TEAD2 are functionally redundant and depend on YAP as coactivator, establishing the genetic logic of the TEAD-YAP module in embryogenesis.

    Evidence Tead1/Tead2 double knockout with Yap genetic epistasis, histology

    PMID:18332127

    Open questions at the time
    • Does not separate TEAD2-specific from TEAD1 functions
    • Direct target genes driving lethality not enumerated
  7. 2010 High

    Provided the structural basis for co-activator dependence by solving the TEAD2 YAP-binding domain fold and mapping the YAP docking surface.

    Evidence X-ray crystallography of YBD, NMR of YAP, in vitro and in vivo binding assays

    PMID:20368466

    Open questions at the time
    • Structure of the full TEAD2-YAP-DNA complex not determined
    • TAZ binding mode not addressed
  8. 2011 High

    Defined an upstream signaling input, showing Yes kinase phosphorylates YAP to activate YAP-TEAD2 transcription required for ES cell self-renewal downstream of LIF.

    Evidence Co-IP, kinase assay, promoter reporters, siRNA, chromatin association at Oct-3/4 promoter

    PMID:21385842

    Open questions at the time
    • Genome-wide TEAD2 targets in ESCs not mapped here
    • Relative contribution of other TEAD paralogs not resolved
  9. 2019 Medium

    Extended TEAD2's chromatin role to lineage specification and identified post-transcriptional regulation, showing Tead2 co-occupies Pax3-bound myogenic elements and is repressed by miR-608 to set drug sensitivity.

    Evidence ChIP-seq/ATAC-seq in Pax3-induced ESCs and embryos; dual-luciferase 3'UTR reporter and rescue in NSCLC

    PMID:30807574 PMID:31485614

    Open questions at the time
    • Tead2 functional contribution to myogenesis inferred from co-occupancy, not loss-of-function
    • miR-608 finding from a single lab
  10. 2022 Medium

    Uncovered a repressive metabolic function, showing TEAD2 with E2A represses acetyl-CoA biosynthesis to drive HCC growth.

    Evidence RNA-seq, siRNA knockdown, acetyl-CoA and acetylation measurements, mouse HCC model

    PMID:36400009

    Open questions at the time
    • Direct promoter occupancy at acetyl-CoA genes not fully mapped
    • Co-activator/co-repressor identity for repression unclear
  11. 2023 High

    Identified TEAD2 as the selectively required TEAD paralog for TAZ-driven tumors and defined its proliferative and angiogenic target programs across cancer types.

    Evidence AAV knockout in floxed mice, ChIP, CRISPRi screen, ATAC/ChIP-seq, in vivo HCC and PDA models

    PMID:36894036 PMID:36907523

    Open questions at the time
    • Mechanism of TEAD2 paralog selectivity for TAZ not defined
    • PDA findings from a single lab
  12. 2024 Medium

    Established TEAD2 as a genome organizer in pluripotency and a driver of therapy resistance, linking it to enhancer-promoter looping in ground-state ESCs and to TAK1-mediated sorafenib resistance.

    Evidence ChIP-seq/ATAC-seq/Hi-C with Tead2 knockout ESCs; ATAC-seq and ChIP at the TAK1 promoter with inhibitor rescue

    PMID:38605224 PMID:39106149

    Open questions at the time
    • How TEAD2 mediates looping independent of CTCF/YY1 mechanistically unresolved
    • TAK1 resistance study single lab
  13. 2024 Low

    Probed YAP/TAZ-independent TEAD2 functions and additional regulators, indicating TEAD1/2 promote neural progenitor lineage progression and cooperate with EGFR-YAP signaling in drug-resistant melanoma.

    Evidence Conditional double knockouts and epistasis (preprint); EGFR/YAP1 inhibitor and knockdown experiments in melanoma

    PMID:39298503 PMID:bio_10.1101_2024.12.19.629472

    Open questions at the time
    • TEAD-INSM1 cooperation not biochemically characterized
    • TEAD2-specific step in melanoma resistance not dissected
    • Neural progenitor work is a preprint
  14. 2025 Low

    Expanded the regulatory and pharmacological landscape, identifying a peptide inhibitor of the TEA domain and an lncRNA modulator of TEAD2 activity.

    Evidence DNA-binding and reporter assays with TEAi peptide and tumor model (preprint); RNA immunoprecipitation and knockdown for lnc81 in granulosa cells

    PMID:40928008 PMID:bio_10.1101_2025.08.31.672803

    Open questions at the time
    • TEAi mechanism of DNA-binding inhibition and nuclear export lacks structural validation
    • lnc81 interaction from single RIP assay without reciprocal validation
  15. 2026 Medium

    Identified an upstream transcriptional activator of TEAD2, showing MEOX1 directly binds the TEAD2 promoter to drive its expression in hepatic fibrosis.

    Evidence Promoter binding with site-specific mutation, CETSA, SPR, knockdown, CCl4 fibrosis model

    PMID:42116734

    Open questions at the time
    • MEOX1-TEAD2 regulation from a single lab
    • Whether this axis operates outside hepatic stellate cells untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How TEAD2 achieves paralog-selective requirement for TAZ-driven and lineage-specific programs, and how it directs CTCF/YY1-independent enhancer-promoter looping, remain unresolved at the mechanistic level.
  • No structural model of TEAD2 engaging chromatin loops
  • Determinants of TEAD2 vs TEAD1/4 functional selectivity unknown
  • Co-repressor identity for TEAD2-mediated metabolic gene repression not defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 5 GO:0003677 DNA binding 4
Localization
GO:0005634 nucleus 3 GO:0000228 nuclear chromosome 1
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-1643685 Disease 4 R-HSA-162582 Signal Transduction 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-4839726 Chromatin organization 1
Partners
E2ALNC81MEOX1PAX3SIX4TAZYAP1
Complex memberships
TEAD-TAZ complexTEAD-YAP complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 Crystal structure of the YAP-binding domain (YBD) of human TEAD2 was solved, revealing an immunoglobulin-like beta-sandwich fold with two extra helix-turn-helix inserts. NMR studies showed that the TEAD-binding domain of YAP is natively unfolded and undergoes localized conformational changes upon TEAD2 binding. In vitro binding and in vivo functional assays defined an extensive conserved surface of TEAD2 YBD as the YAP-binding site. X-ray crystallography, NMR spectroscopy, in vitro binding assays, in vivo functional assays Proceedings of the National Academy of Sciences of the United States of America High 20368466
2011 TEAD2 and its transcriptional co-activator YAP cooperate in a signaling pathway downstream of the tyrosine kinase Yes in mouse embryonic stem cells. Kinase-active Yes binds and phosphorylates YAP, activates YAP-TEAD2-dependent transcription, and this pathway is required downstream of LIF for ES cell self-renewal. TEAD2 was shown to associate directly with the Oct-3/4 promoter, and activation of the Yes-YAP-TEAD2 pathway induced Oct-3/4 and Nanog promoter activity. Co-immunoprecipitation, kinase assay, promoter-reporter assays, siRNA knockdown, chromatin association assay Journal of cell science High 21385842
2008 Tead1 and Tead2 are functionally redundant in mouse embryonic development. Tead1−/−;Tead2−/− double-knockout embryos die at E9.5 with severe growth defects, lack of notochord maintenance, and defects in yolk sac vasculature. Genetic interaction experiments demonstrated that Tead1 and Tead2 use YAP as a major coactivator in vivo. Double-knockout embryos showed reduced cell proliferation and increased apoptosis. Mouse knockout genetics, genetic epistasis with Yap mutants, histological and molecular analysis Molecular and cellular biology High 18332127
2004 Tead2 binds to a neural crest enhancer element in the Pax3 genomic locus and activates Pax3 expression. Mutation of the Tead2 binding site in Pax3 transgenic constructs abolished neural expression. A Tead2-Engrailed repressor fusion suppressed Pax3 expression in P19 cells and in vivo. Tead2 and its co-activator YAP65 are co-expressed with Pax3 in the dorsal neural tube. Transgenic mouse reporter assays, co-transfection, dominant-negative Tead2-Engrailed fusion, site-directed mutagenesis of binding site Development (Cambridge, England) High 14736747
2005 Tead2 directly activates the Fgfr4 promoter through an M-CAT motif (5'-CATTCCT-3'). Mutation of this M-CAT motif abolished Tead2-driven Fgfr4 promoter activity in co-transfection assays. MyoD directly bound two E-boxes in the first intron of Tead2 (by ChIP), and co-transfection of MyoD activated Tead2 intronic reporter activity in a dose-dependent manner, establishing a MyoD-Tead2-Fgfr4 transcriptional pathway required for muscle regeneration. Co-transfection/promoter-reporter assay, site-directed mutagenesis of M-CAT, chromatin immunoprecipitation (ChIP), immunostaining The Journal of biological chemistry High 16267055
2007 Inactivation of the Tead2 gene in mice significantly increased the risk of exencephaly (defect in neural tube closure). This role in neural tube closure was found to be independent of Pax3 regulation, as Pax3 expression was normal in E11.5 Tead2 nullizygous embryos. The risk of exencephaly was greatest with Tead2 nullizygous females and could be suppressed by folic acid or pifithrin-alpha, revealing a maternal genetic contribution. Mouse knockout, phenotypic analysis, pharmacological rescue (folic acid, pifithrin-alpha) Genesis (New York, N.Y. : 2000) Medium 17868131
1989 Transcription factor ETF (TEAD2) specifically stimulates transcription from promoters lacking a TATA box. ETF recognizes GC-rich sequences including GC boxes and TATA boxes (with lower affinity). ETF-binding sites only functionally activated transcription when placed upstream of TATA-less promoters; introduction of a TATA box into the EGFR promoter abolished ETF responsiveness. In vitro transcription assay, DNA binding (gel-shift), promoter-reporter analysis with TATA box substitution The Journal of biological chemistry High 2768275
1999 ETF (TEAD2) binds to three upstream and one downstream site in the mouse p53 promoter, and adenovirus E1a proteins stimulate this binding to transcriptionally activate the p53 gene. The ETF site downstream of the transcription start site was identified as the key element conferring E1a responsiveness. Both major E1a proteins (243R and 289R) were required for complete activation. Promoter-reporter assay, electrophoretic mobility shift assay (EMSA), deletion/mutation analysis The Journal of biological chemistry Medium 10446138
2022 TEAD2 (together with E2A) transcriptionally represses all six acetyl-CoA biosynthesis pathways in hepatocellular carcinoma, leading to decreased acetyl-CoA levels and hypo-acetylation of non-histone proteins. Knockdown of TEAD2 restored acetyl-CoA levels and inhibited tumor growth in a mouse HCC model. RNA sequencing, mouse HCC model, siRNA knockdown, metabolic measurements of acetyl-CoA levels and protein acetylation Molecular cell Medium 36400009
2023 In hepatocellular carcinoma, TAZ-driven tumor growth specifically requires TEAD2 (and to a lesser extent TEAD4). TAZ and TEAD2 promote HCC proliferation via transcriptional upregulation of ANLN and KIF23, as confirmed by chromatin immunoprecipitation and CRISPRi screen. TAZ expression in HCC is regulated by cholesterol synthesis upstream of TEAD2. AAV-mediated knockout in floxed mice, RNA-seq, ChIP, CRISPRi screen, TAZ-S89A overexpression HCC model Gastroenterology High 36894036
2023 In basal-like pancreatic ductal adenocarcinoma (PDA) cells, TEAD2 drives a proangiogenic enhancer landscape. Genetic and pharmacologic inhibition of TEAD2 impairs proangiogenic phenotypes in vitro and cancer progression in vivo. CD109 was identified as a critical TEAD2 downstream mediator that maintains constitutively activated JAK-STAT signaling in basal-like PDA cells. Epigenome analysis (ATAC-seq/ChIP-seq), transcriptome analysis, loss-of-function (genetic and pharmacologic), in vivo tumor models Gastroenterology Medium 36907523
2024 TEAD2 binds to the TAK1 promoter and transcriptionally activates TAK1 expression, thereby mediating sorafenib resistance in hepatocellular carcinoma. Functional assays showed that TEAD2 promotes HCC progression and drug resistance, and TAK1 inhibitors reversed TEAD2-induced sorafenib resistance. Accessibility sequencing (ATAC-seq), chromatin immunoprecipitation for TAK1 promoter, functional cell-based assays, TAK1 inhibitor treatment Molecular cancer research : MCR Medium 39106149
2024 TEAD2 exhibits increased chromatin binding in ground-state (2i/LIF) mouse embryonic stem cells, targeting active chromatin regions to regulate 2i-specific gene expression. TEAD2 mediates enhancer-promoter looping interactions during the serum/LIF to 2i/LIF transition. Deletion of Tead2 reduces a specific set of enhancer-promoter interactions without significantly affecting CTCF or YY1 binding. ChIP-seq, ATAC-seq, Hi-C/chromatin interaction assays, Tead2 knockout ESCs The EMBO journal High 38605224
2019 TEAD2 mRNA is a direct target of miR-608 in NSCLC cells, as confirmed by dual-luciferase reporter assay. miR-608 overexpression negatively regulated TEAD2 protein levels and decreased expression of Hippo-YAP pathway target genes. Restoration of TEAD2 reversed the increased cisplatin sensitivity induced by miR-608, placing TEAD2 downstream of miR-608 in mediating drug sensitivity. Dual-luciferase reporter assay, western blot, siRNA/overexpression rescue experiments Molecular medicine reports Medium 31485614
2019 Pax3 cooperates with Six4 and Tead2 at chromatin to specify the skeletal myogenic lineage. ChIP-seq and ATAC-seq in Pax3-induced embryonic stem cells and Pax3-null E9.5 mouse embryos showed that Pax3 binding increases chromatin accessibility and that Tead2 co-occupies Pax3-bound elements in the context of myogenic specification. ChIP-seq, ATAC-seq, RNA-seq, Pax3-null mouse embryo analysis, ES cell differentiation platform PLoS biology Medium 30807574
2001 A 117-bp enhancer in the first intron of the mouse ETF/Tead2 gene is required for cell-specific transcriptional activation. This enhancer contains a GC box and two GA elements. Sp1 acts as an activator by competing with an unknown repressor (GA element-binding factor) for binding to the GC box and GA elements to achieve full enhancer activity. Transient transfection assays, electrophoretic mobility shift assays (EMSA), deletion and point mutation analysis Biochemical and biophysical research communications Medium 11741291
2024 In vemurafenib-resistant melanoma cells, EGFR signaling activates YAP1 nuclear localization, which in turn cooperates with TEAD2 to upregulate STIM1 expression. EGF and EGFR levels are increased in resistant cells, and this pathway drives STIM1-dependent calcium entry associated with drug resistance. Pathway inhibitor experiments, YAP1 nuclear localization assays, gene knockdown, reporter/expression analysis The FEBS journal Low 39298503
1998 ETF (TEAD2/mETF) encodes a full-length protein with a TEA/ATTS DNA-binding domain. Gel mobility shift assays confirmed that ETF binds M-CAT/GT-IIC elements, and GAL4-fusion protein analysis demonstrated that ETF contains a transcriptional activation domain. cDNA cloning, gel mobility shift assay, GAL4 fusion transcription activation assay DNA and cell biology Medium 9502435
2025 A peptide inhibitor (TEAi) derived from Drosophila Nerfin-1 directly binds the TEA DNA-binding domain of TEAD2 and inhibits its DNA-binding capacity without direct DNA interaction, thereby abolishing promoter recruitment of the TEAD-YAP complex. TEAi also induced nuclear export and cytoplasmic accumulation of TEAD2, suggesting a non-canonical mechanism. TEAi suppressed TEAD-YAP-driven transcriptional activity (CTGF, CYR61) and tumor growth in vivo. Luciferase reporter assay, qPCR, DNA-binding assay, nuclear/cytoplasmic fractionation, in vivo tumor model bioRxivpreprint Low bio_10.1101_2025.08.31.672803
2024 TEAD1/2 have both YAP/TAZ-dependent and YAP/TAZ-independent functions during ventral telencephalon development in mice. Whereas YAP/TAZ loss depletes early progenitors, TEAD1/2 loss expands early progenitors and reduces late progenitors, indicating that TEAD1/2 promote neural progenitor lineage progression. TEAD1/2 do so in part by inhibiting Notch signaling and cooperating with INSM1. Mouse conditional double knockout (TEAD1/2 and YAP/TAZ), histological and molecular analysis, epistasis experiments bioRxivpreprint Low bio_10.1101_2024.12.19.629472
2025 lnc81 physically interacts with TEAD2 in ovarian granulosa cells, as shown by RNA immunoprecipitation (RIP), and is predominantly nuclear. lnc81 knockdown upregulates CCN1/CCN2 protein levels without affecting TEAD2 protein expression, suggesting lnc81 modulates TEAD2 transcriptional activity rather than its stability. RNA immunoprecipitation (RIP), subcellular fractionation, siRNA knockdown, western blot Journal of cellular physiology Low 40928008
2026 MEOX1 promotes TEAD2 transcription by binding to the -988 to -982 nt region of the TEAD2 promoter, as demonstrated by molecular docking and site-specific mutation experiments, establishing MEOX1 as a direct transcriptional activator of TEAD2. Knockdown of MEOX1 decreased TEAD2 expression and reduced Hippo pathway target transcription and hepatic stellate cell activation. Promoter binding assay with site-specific mutation, CETSA, surface plasmon resonance, siRNA knockdown, in vivo CCl4 fibrosis model British journal of pharmacology Medium 42116734

Source papers

Stage 0 corpus · 58 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 Coupled ferredoxin and crotonyl coenzyme A (CoA) reduction with NADH catalyzed by the butyryl-CoA dehydrogenase/Etf complex from Clostridium kluyveri. Journal of bacteriology 305 17993531
2003 Clear relationship between ETF/ETFDH genotype and phenotype in patients with multiple acyl-CoA dehydrogenation deficiency. Human mutation 191 12815589
2011 Regulation of mouse embryonic stem cell self-renewal by a Yes-YAP-TEAD2 signaling pathway downstream of LIF. Journal of cell science 182 21385842
1989 Nuclear factor ETF specifically stimulates transcription from promoters without a TATA box. The Journal of biological chemistry 160 2768275
2008 Redundant roles of Tead1 and Tead2 in notochord development and the regulation of cell proliferation and survival. Molecular and cellular biology 151 18332127
2010 Structural and functional analysis of the YAP-binding domain of human TEAD2. Proceedings of the National Academy of Sciences of the United States of America 140 20368466
2013 Studies on the mechanism of electron bifurcation catalyzed by electron transferring flavoprotein (Etf) and butyryl-CoA dehydrogenase (Bcd) of Acidaminococcus fermentans. The Journal of biological chemistry 105 24379410
2004 Identification of minimal enhancer elements sufficient for Pax3 expression in neural crest and implication of Tead2 as a regulator of Pax3. Development (Cambridge, England) 93 14736747
2002 Glutaric acidemia type II: gene structure and mutations of the electron transfer flavoprotein:ubiquinone oxidoreductase (ETF:QO) gene. Molecular genetics and metabolism 92 12359134
2005 Fgfr4 is required for effective muscle regeneration in vivo. Delineation of a MyoD-Tead2-Fgfr4 transcriptional pathway. The Journal of biological chemistry 86 16267055
2010 Transcription factors ETF, E2F, and SP-1 are involved in cytokine-independent proliferation of murine hepatocytes. Hepatology (Baltimore, Md.) 84 20979052
2012 Molecular mechanisms of riboflavin responsiveness in patients with ETF-QO variations and multiple acyl-CoA dehydrogenation deficiency. Human molecular genetics 78 22611163
2007 Transcription factor TEAD2 is involved in neural tube closure. Genesis (New York, N.Y. : 2000) 75 17868131
2023 A Therapeutically Targetable TAZ-TEAD2 Pathway Drives the Growth of Hepatocellular Carcinoma via ANLN and KIF23. Gastroenterology 62 36894036
2016 Ehrlichia secretes Etf-1 to induce autophagy and capture nutrients for its growth through RAB5 and class III phosphatidylinositol 3-kinase. Autophagy 61 27541856
2016 An evolutionary, structural and functional overview of the mammalian TEAD1 and TEAD2 transcription factors. Gene 49 27421669
1995 Phylogenetic characterization of the ubiquitous electron transfer flavoprotein families ETF-alpha and ETF-beta. Research in microbiology 46 8525056
2018 Ehrlichia type IV secretion system effector Etf-2 binds to active RAB5 and delays endosome maturation. Proceedings of the National Academy of Sciences of the United States of America 45 30181274
2007 Impact of mutations on the midpoint potential of the [4Fe-4S]+1,+2 cluster and on catalytic activity in electron transfer flavoprotein-ubiquinone oxidoreductase (ETF-QO). Biochemistry 32 18069858
2021 ETF dehydrogenase advances in molecular genetics and impact on treatment. Critical reviews in biochemistry and molecular biology 31 33823724
2000 Soggy, a spermatocyte-specific gene, lies 3.8 kb upstream of and antipodal to TEAD-2, a transcription factor expressed at the beginning of mouse development. Nucleic acids research 31 11024178
2020 Optimization of electrotransformation (ETF) conditions in lactic acid bacteria (LAB). Journal of microbiological methods 28 32417130
2019 Time-dependent Pax3-mediated chromatin remodeling and cooperation with Six4 and Tead2 specify the skeletal myogenic lineage in developing mesoderm. PLoS biology 27 30807574
2022 Transcription factors TEAD2 and E2A globally repress acetyl-CoA synthesis to promote tumorigenesis. Molecular cell 25 36400009
2022 YY1-induced DLEU1/miR-149-5p Promotes Malignant Biological Behavior of Cholangiocarcinoma through Upregulating YAP1/TEAD2/SOX2. International journal of biological sciences 23 35864972
1999 The adenovirus oncoprotein E1a stimulates binding of transcription factor ETF to transcriptionally activate the p53 gene. The Journal of biological chemistry 22 10446138
2010 Novel ETF dehydrogenase mutations in a patient with mild glutaric aciduria type II and complex II-III deficiency in liver and muscle. Journal of inherited metabolic disease 19 21088898
2000 Formation of W(3)A(1) electron-transferring flavoprotein (ETF) hydroquinone in the trimethylamine dehydrogenase x ETF protein complex. The Journal of biological chemistry 19 10777543
2019 MicroRNA‑608 sensitizes non‑small cell lung cancer cells to cisplatin by targeting TEAD2. Molecular medicine reports 18 31485614
2019 ETF-QO Mutants Uncoupled Fatty Acid β-Oxidation and Mitochondrial Bioenergetics Leading to Lipid Pathology. Cells 17 30709034
2023 A TEAD2-Driven Endothelial-Like Program Shapes Basal-Like Differentiation and Metastasis of Pancreatic Cancer. Gastroenterology 13 36907523
2012 Mutations at the flavin binding site of ETF:QO yield a MADD-like severe phenotype in Drosophila. Biochimica et biophysica acta 13 22580358
2007 Electron spin relaxation enhancement measurements of interspin distances in human, porcine, and Rhodobacter electron transfer flavoprotein-ubiquinone oxidoreductase (ETF-QO). Journal of magnetic resonance (San Diego, Calif. : 1997) 13 18037314
1996 Structural organization and chromosomal assignment of the mouse embryonic TEA domain-containing factor (ETF) gene. Genomics 11 8812452
2021 Exploring TEAD2 as a drug target for therapeutic intervention of cancer: A multi-computational case study. Briefings in bioinformatics 10 33611407
2020 Conformational analysis of the riboflavin-responsive ETF:QO-p.Pro456Leu variant associated with mild multiple acyl-CoA dehydrogenase deficiency. Biochimica et biophysica acta. Proteins and proteomics 10 32087359
2008 Probing the dynamic interface between trimethylamine dehydrogenase (TMADH) and electron transferring flavoprotein (ETF) in the TMADH-2ETF complex: role of the Arg-alpha237 (ETF) and Tyr-442 (TMADH) residue pair. Biochemistry 9 18407658
2024 EGF/EGFR-YAP1/TEAD2 signaling upregulates STIM1 in vemurafenib resistant melanoma cells. The FEBS journal 8 39298503
2023 Inhibition of Ehrlichia chaffeensis infection by cell-permeable macrocyclic peptides that bind type IV secretion effector Etf-1. PNAS nexus 8 36874272
2022 Electron Transfer Flavoprotein (ETF) α Controls Blood Vessel Development by Regulating Endothelial Mitochondrial Bioenergetics and Oxygen Consumption. Oxidative medicine and cellular longevity 7 35313640
2024 Ehrlichia chaffeensis Etf-3 Induces Host RAB15 Upregulation for Bacterial Intracellular Growth. International journal of molecular sciences 4 38473798
2024 Development of Etf-3-specific nanobodies to prevent Ehrlichia infection and LNP-mRNA delivery in cellular and murine models. Microbiological research 4 39705831
2020 Three-dimensional analyses of cells' positioning on the quadrupole-electrode microfluid chip considering the coupling effect of nDEP, ACEO, and ETF. Biosensors & bioelectronics 4 32729519
1999 Assignment of electron transfer flavoprotein-ubiquinone oxidoreductase (ETF-QO) to human chromosome 4q33 by fluorescence in situ hybridization and somatic cell hybridization. Molecular genetics and metabolism 4 10444348
2024 TEAD2 initiates ground-state pluripotency by mediating chromatin looping. The EMBO journal 3 38605224
2021 CHIP control degradation of mutant ETF:QO through ubiquitylation in late-onset multiple acyl-CoA dehydrogenase deficiency. Journal of inherited metabolic disease 3 33438237
2001 Identification and characterization of cell-specific enhancer elements for the mouse ETF/Tead2 gene. Biochemical and biophysical research communications 3 11741291
2024 TEAD2 Promotes Hepatocellular Carcinoma Development and Sorafenib Resistance via TAK1 Transcriptional Activation. Molecular cancer research : MCR 2 39106149
1999 5,5'-Dithiobis-(2-nitrobenzoic acid) as a probe for a non-essential cysteine residue at the medium chain acyl-coenzyme A dehydrogenase binding site of the human 'electron transferring flavoprotein' (ETF). Journal of enzyme inhibition 2 10488248
1998 cDNA cloning and characterization of mouse DTEF-1 and ETF, members of the TEA/ATTS family of transcription factors. DNA and cell biology 2 9502435
1994 Impaired degradation of phytanic acid in cells from patients with mitochondriopathies: evidence for the involvement of ETF and the respiratory chain in phytanic acid alpha-oxidation. Journal of inherited metabolic disease 1 7837758
2026 Conversion of a bifurcating ETF to a canonical ETF by site-directed mutagenesis. Archives of biochemistry and biophysics 0 42035820
2026 Mitochondrial ETF insufficiency drives neoplastic growth by selectively optimizing cancer bioenergetics. eLife 0 42085321
2026 Ligustilide alleviates hepatic fibrosis by targeting the mesenchymal homeobox 1 (MEOX1)- transcriptional enhanced associate domain factor 2 (TEAD2) signalling axis. British journal of pharmacology 0 42116734
2026 Machine Learning-Based Study on Xin-Pi Simultaneous Treatment Formula via Drug Nanodelivery Systems Regulating Macrophage Polarization and TEAD2/PKM2 Synergistic Repair Strategy in Myocarditis. SLAS technology 0 42150704
2026 Exercise based Intervention For Metabolic Inflexibility Linked With Lipid Storage Myopathy Using Innovative CRISPR Etf-QO Mutant Knock-in Models. bioRxiv : the preprint server for biology 0 42239388
2025 Genotype-Phenotype Correlation of ETF Dehydrogenase Gene-Related Multiple Acyl-CoA Dehydrogenation Deficiency in Chinese Patients. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 40827880
2025 The Age-Associated Long Noncoding RNA lnc81 Regulates Ovarian Granulosa Cell Proliferation and Apoptosis Through TEAD2-CCN1/2 Pathway in Mice. Journal of cellular physiology 0 40928008

Missed literature

Know a paper Affinage missed for TEAD2? Flag it for the maintainers and the community.

No submissions yet.