Affinage

TCF7L1

Transcription factor 7-like 1 · UniProt Q9HCS4

Round 2 corrected
Length
588 aa
Mass
62.6 kDa
Annotated
2026-04-28
130 papers in source corpus 41 papers cited in narrative 41 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TCF7L1 (formerly Tcf3) is an HMG-box transcription factor that functions as a constitutive repressor of Wnt target genes and pluripotency regulators, thereby governing the balance between stem cell self-renewal and lineage specification across multiple tissues. TCF7L1 represses target genes—including Nanog, Esrrb, Tbx3, Lef1, FoxA2, and Neurogenin1—by recruiting Groucho/TLE–HDAC1 co-repressor complexes to their promoters, and this repression maintains heterochromatin marks (reduced H3 acetylation, elevated H3K9me3) genome-wide (PMID:16894029, PMID:18483421, PMID:21666599, PMID:21730189). Wnt/β-catenin signaling inactivates TCF7L1 not by converting it into a coactivator but by recruiting HIPK2 to phosphorylate TCF7L1, causing its dissociation from DNA and subsequent protein degradation, which enables replacement by positively acting TCF1/LEF1 at target promoters (PMID:20951344, PMID:21285352, PMID:23810553). Missense variants in TCF7L1 with reduced repressor activity have been identified in patients with congenital hypopituitarism, establishing a direct link between impaired TCF7L1 repression and human hypothalamo-pituitary developmental disease (PMID:26764381).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2000 High

    Structural resolution of the β-catenin–TCF7L1 interface established the atomic basis for how TCF7L1 engages the Wnt effector β-catenin through an elongated binding domain occupying the armadillo repeat groove, revealing shared and competing binding sites with APC, Axin, and cadherins.

    Evidence X-ray crystallography of β-catenin bound to the TCF7L1 catenin-binding domain, with structure-based mutagenesis

    PMID:11136974

    Open questions at the time
    • Structure did not resolve the HMG-box DNA-binding domain or full-length protein
    • No information on how post-translational modifications alter the interaction interface
  2. 2000 High

    The zebrafish headless mutant demonstrated that TCF7L1 functions in vivo as a transcriptional repressor of Wnt target genes essential for vertebrate head formation, establishing its identity as a default repressor rather than an activator in the Wnt pathway.

    Evidence Zebrafish forward genetic screen and loss-of-function mutant phenotyping

    PMID:11057671

    Open questions at the time
    • Downstream target genes were not individually identified
    • Whether repression was Groucho-dependent was not tested
  3. 2001 High

    Biochemical studies revealed that TCF7L1 competes with Axin/APC for β-catenin binding and that CK1ε phosphorylation stimulates this interaction, while identification of Groucho/TLE–HDAC1 as obligate co-repressors defined the molecular machinery through which TCF7L1 silences target genes.

    Evidence Xenopus extract competition binding assays, in vitro kinase assays, co-immunoprecipitation and reporter assays across TCF/LEF family members

    PMID:11266540 PMID:11524435

    Open questions at the time
    • Endogenous chromatin occupancy was not assessed
    • Relative contributions of CK1ε versus other kinases in vivo were unclear
  4. 2006 High

    ChIP and knockout studies in embryonic stem cells and adult skin established that TCF7L1 directly binds and represses the Nanog promoter and maintains an undifferentiated stem cell state by silencing differentiation programs in a Groucho-interaction-domain-dependent manner.

    Evidence Chromatin immunoprecipitation, promoter reporter assays, Tcf3 knockout ESCs, inducible transgenic mouse skin system

    PMID:16894029 PMID:17018284

    Open questions at the time
    • Genome-wide target repertoire was not yet mapped
    • How Wnt signaling quantitatively tunes TCF7L1 occupancy at Nanog was unresolved
  5. 2008 High

    Genome-wide ChIP and transcriptomics in ESCs demonstrated that TCF7L1 acts broadly to repress multiple self-renewal genes (Nanog, Tcl1, Tbx3, Esrrb) without affecting Oct4 or Sox2, redefining it as a cell-intrinsic inhibitor of the entire pluripotency network rather than a single-gene repressor.

    Evidence Genome-wide ChIP-chip and transcriptome analysis in Tcf3 knockout ESCs

    PMID:18483421

    Open questions at the time
    • Whether TCF7L1 directly or indirectly repressed each target was not fully resolved
    • Epigenomic consequences of TCF7L1 binding were not characterized
  6. 2010 High

    The discovery that Wnt-stimulated β-catenin recruits HIPK2 to phosphorylate TCF7L1, causing its dissociation from DNA, overturned the classical coactivator-switch model and established a 'removal' mechanism as the primary mode of TCF7L1 inactivation during Wnt signaling.

    Evidence Xenopus embryo phosphorylation assays, co-immunoprecipitation, ChIP, phospho-resistant mutant analysis

    PMID:20951344

    Open questions at the time
    • Specific HIPK2 phosphorylation sites on TCF7L1 were not mapped
    • Whether HIPK2-mediated removal operates in all cell types was untested
  7. 2011 High

    A convergence of studies established the TCF-switching paradigm: HIPK2-mediated TCF7L1 phosphorylation causes its replacement by activating TCF1 at target promoters; genetic ablation of Tcf3 replaced the requirement for Wnt3a in ESC self-renewal; and Groucho/TLE–HDAC1 co-repressors were shown to be essential for TCF7L1 repression at targets like cdx4, with E4f1 capable of displacing co-repressors without affecting DNA binding.

    Evidence HIPK2 kinase-dead constructs and ChIP in Xenopus; Tcf3 genetic knockout with ChIP in ESCs; zebrafish co-repressor epistasis

    PMID:21285352 PMID:21666599 PMID:21685894

    Open questions at the time
    • How TCF1 is selectively recruited to vacated sites was mechanistically unclear
    • Whether the TCF switch requires additional chromatin remodeling factors was not addressed
  8. 2011 Medium

    Tcf3 knockout ESCs showed genome-wide increases in H3 acetylation and decreases in H3K9me3, revealing that TCF7L1 repression maintains heterochromatin marks and explaining how its absence dramatically enhances somatic cell reprogramming efficiency.

    Evidence Chromatin immunofluorescence and reprogramming assays in Tcf3 knockout ESCs

    PMID:21730189

    Open questions at the time
    • Whether epigenomic changes are direct consequences of TCF7L1 binding or secondary effects was not resolved
    • Genome-wide ChIP-seq for histone marks in knockout cells was not performed
  9. 2012 High

    A β-catenin-interaction-deficient knock-in mouse (Tcf3ΔN) progressed through gastrulation normally, genetically proving that TCF7L1's primary repressor function during gastrulation is β-catenin-independent; post-gastrulation, β-catenin interaction indirectly activates targets by de-repressing Lef1, which then activates genes via Lef1–β-catenin complexes.

    Evidence Knock-in mouse genetics with developmental phenotyping and epistasis analysis

    PMID:22573616

    Open questions at the time
    • How TCF7L1 represses Lef1 mechanistically (direct binding versus indirect) was not dissected at the chromatin level
    • Whether this indirect activation model applies to all post-gastrulation contexts was unknown
  10. 2012 High

    Identification of Esrrb as the pivotal target repressed by TCF7L1 downstream of GSK3 inhibition, where forced Esrrb expression is sufficient to replace GSK3 inhibition or Tcf3 deletion for ESC self-renewal, defined the minimal effector axis linking Wnt signaling to pluripotency maintenance.

    Evidence Genome localization, transcriptome analysis, knockdown/knockout and forced expression in ESCs

    PMID:23040478

    Open questions at the time
    • Whether Esrrb sufficiency extends to in vivo contexts was not tested
    • Other TCF7L1 targets may contribute to self-renewal in parallel
  11. 2013 High

    β-catenin was shown to inactivate TCF7L1 by promoting its removal from DNA and subsequent protein degradation rather than by forming a coactivator complex, with mouse genetics demonstrating that TCF7L1 inactivation is the sole required output of the TCF7L1–β-catenin interaction.

    Evidence Mouse knock-in alleles, ChIP, protein stability assays

    PMID:23810553

    Open questions at the time
    • The ubiquitin ligase responsible for TCF7L1 degradation was not identified
    • Whether degradation is proteasome-dependent was not directly shown
  12. 2014 High

    TCF7L1 was found to promote wound healing via a β-catenin-independent, non-cell-autonomous mechanism in skin keratinocytes, with LCN2 identified as the secreted effector and Stat3 as an upstream activator, revealing a Wnt-independent wound repair function.

    Evidence Gain/loss-of-function in keratinocytes and mouse wound healing models, secretome analysis

    PMID:24909826

    Open questions at the time
    • How TCF7L1 transcriptionally activates LCN2 (direct binding versus indirect) was not established
    • Whether this pathway operates in non-cutaneous wound repair was unknown
  13. 2016 High

    Human TCF7L1 variants (p.R92P, p.R400Q) with reduced repressor activity were identified in patients with congenital hypopituitarism, and conditional mouse knockouts confirmed that TCF7L1 repressor function in the prospective hypothalamus is essential for Rathke's pouch induction independently of β-catenin interaction.

    Evidence Conditional mouse knockout, human patient variant identification and functional validation in vitro and in vivo

    PMID:26764381

    Open questions at the time
    • Penetrance and expressivity of TCF7L1 variants in larger patient cohorts was not assessed
    • Precise target genes repressed by TCF7L1 in hypothalamic development were not identified
  14. 2019 High

    Triple deletion of Etv5, Rbpj, and Tcf3 locked ESCs in self-renewal under differentiation conditions, demonstrating that TCF7L1 functions alongside FGF- and Notch-pathway repressors as a driver of the naive-to-formative pluripotency transition.

    Evidence Triple gene deletion with genome-wide transcriptomics and ESC differentiation assays

    PMID:31031137

    Open questions at the time
    • Whether these three factors converge on shared target genes or act in parallel was not resolved
    • The formative state was defined transcriptomically but not functionally in vivo
  15. 2023 High

    Time-series genomics established that TCF7L1 transcriptional repression promotes primitive endoderm differentiation by directly repressing naive pluripotency factors and formative regulators including Otx2 and Lef1, while its deletion specifically abrogates primitive endoderm without restraining epiblast priming.

    Evidence RNA-seq time-series, ChIP, Tcf7l1 conditional knockout, ESC differentiation and preimplantation embryo analysis

    PMID:36869101

    Open questions at the time
    • Whether TCF7L1 represses distinct target sets in primitive endoderm versus epiblast lineages was not fully dissected
    • Upstream signals that modulate TCF7L1 occupancy during preimplantation were not identified
  16. 2024 High

    In CD8+ T cells, Id2 disrupts a TCF7L1–Tal1–LSD1 complex at the Slamf6 promoter, preventing LSD1-mediated H3K4me2 demethylation and epigenetically promoting progenitor exhausted T cell fate, revealing a TCF7L1 repressor function in adaptive immunity.

    Evidence Co-immunoprecipitation, ChIP-seq, ATAC-seq, Id2 knockout with LSD1 inhibitor rescue

    PMID:38287103

    Open questions at the time
    • Whether TCF7L1 partners with LSD1 at other immune gene loci is unknown
    • The generality of TCF7L1 function in T cell biology beyond the exhaustion context has not been explored

Open questions

Synthesis pass · forward-looking unresolved questions
  • The ubiquitin ligase(s) responsible for TCF7L1 degradation upon Wnt-stimulated removal from DNA, the full structural basis of the HMG-box domain on chromatin, and whether the TCF-switching mechanism operates uniformly across all TCF7L1-expressing tissues remain unresolved.
  • No E3 ligase for TCF7L1 turnover has been identified
  • No full-length TCF7L1 structure exists
  • Tissue-specific modulation of the TCF switch is uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 17 GO:0003677 DNA binding 9 GO:0098772 molecular function regulator activity 3
Localization
GO:0005634 nucleus 8
Pathway
R-HSA-74160 Gene expression (Transcription) 10 R-HSA-1266738 Developmental Biology 8 R-HSA-4839726 Chromatin organization 2
Partners
CTNNB1E4F1HDAC1HIPK2JMJD6LSD1TAL1TLE1
Complex memberships
Groucho/TLE-HDAC1 co-repressor complexTCF7L1–Tal1–LSD1 complexTCF7L1–β-catenin complex

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 Crystal structure of β-catenin bound to the β-catenin-binding domain of Tcf3 (Tcf7l1) revealed that the Tcf3-CBD forms an elongated structure with three binding modules running antiparallel to β-catenin along the positively charged groove of the armadillo repeats; structure-based mutagenesis defined three sites in β-catenin critical for Tcf3-CBD binding that are differentially involved in binding APC, cadherin, and Axin. X-ray crystallography + structure-based mutagenesis Cell High 11136974
2000 Loss-of-function of zebrafish Tcf3 (headless mutant) reveals that Tcf3 functions as a transcriptional repressor of Wnt target genes and is essential for vertebrate head formation; genetic evidence places Tcf3 as a repressor downstream of Wnt signaling during anterior patterning. Zebrafish forward genetic screen, loss-of-function mutant analysis Nature High 11057671
2001 Tcf3 (Tcf7l1) competes with Axin and APC for β-catenin binding, thereby inhibiting β-catenin turnover; CK1ε phosphorylates Tcf3 to stimulate its binding to β-catenin (an effect reversed by GSK3), and Tcf3 synergizes with CK1ε to inhibit β-catenin degradation; a significant fraction of Tcf3 protein is non-nuclear. Xenopus embryo extract biochemistry, competition binding assays, in vitro kinase assays The Journal of Cell Biology High 11524435
2001 All TCF/LEF family members, including Tcf3, interact with Groucho (TLE/Grg) co-repressors; 'long' Groucho family members repress Tcf-mediated transactivation via interaction with HDAC1, while Grg-5 (short form) acts as a de-repressor; redundancy in Tcf/Grg interactions is the rule within cell lines. Reporter assays, co-immunoprecipitation, expression profiling of cell lines Nucleic Acids Research High 11266540
2001 I-mfa domain proteins (I-mfa and Xenopus XIC) inhibit the DNA binding and transcriptional activity of XTcf3 in Xenopus embryos, blocking dorsal axis specification and repressing Tcf3/β-catenin-regulated target genes (siamois, Xnr3); ectopic expression of I-mfa inhibited the ability of β-catenin to activate Lef/Tcf reporter constructs. Xenopus embryo overexpression, reporter assays, ectopic axis induction assays Molecular and Cellular Biology Medium 11238923
2002 In Xenopus development, XTcf-3 function is specifically required for early maternal Wnt signaling to establish the dorsal embryonic axis, while closely related XLef-1 mediates zygotic Wnt signaling to pattern the mesoderm; this demonstrates that different Lef/Tcf family members mediate tissue-specific Wnt responses in the same pathway. Xenopus loss-of-function (dominant negative constructs, morpholinos), gain-of-function, embryological assays Current Biology Medium 12445388
2002 Tcf3 binds directly to a distal TCF binding site in the Xenopus myf-5 regulatory region and represses myf-5 transcription in midline mesoderm; endogenous Wnt signaling in lateral mesoderm is required to overcome this Tcf3-mediated long-range repression. Transgenic reporter assay, in vitro DNA binding (gel shift), Xenopus embryo analysis Mechanisms of Development Medium 12049769
2006 Tcf3 directly binds to the Nanog gene promoter regulatory region and represses its transcriptional activity in embryonic stem cells through a Groucho interaction domain-dependent process; absence of Tcf3 elevates Nanog mRNA, protein and promoter activity and delays differentiation. Chromatin immunoprecipitation, promoter reporter assays, Tcf3 knockout ESCs Molecular and Cellular Biology High 16894029
2006 In adult skin, Tcf3 maintains an undifferentiated stem cell state by repressing transcriptional regulators of epidermal, sebaceous gland, and hair follicle differentiation programs; upon Wnt signaling, Tcf3-expressing stem cells are directed along the hair lineage. Inducible Tcf3 reactivation in committed epidermal cells induces genes associated with an undifferentiated, Wnt-inhibited state. Inducible transgenic mouse system, gain- and loss-of-function in vivo Cell High 17018284
2008 Tcf3 acts broadly on a genome-wide scale in ESCs to reduce levels of multiple self-renewal promoters (Nanog, Tcl1, Tbx3, Esrrb) while not affecting Oct4 or Sox2; Tcf3 counteracts effects of both Nanog and Oct4, functioning as a cell-intrinsic inhibitor of pluripotent cell self-renewal. Genome-wide ChIP, transcriptome analysis, Tcf3 knockout ESCs, knockdown comparisons Stem Cells High 18483421
2009 In zebrafish spinal cord, Tcf3 represses sox4a expression to inhibit premature neurogenesis in spinal progenitors, and regulates Dbx gene expression in intermediate progenitors; both functions are mediated independently of canonical Wnt signaling. Zebrafish loss-of-function, in situ hybridization, epistasis with Wnt pathway components Development Medium 19176587
2010 Wnt proteins stimulate TCF3 phosphorylation in gastrulating Xenopus embryos and mammalian cells; this phosphorylation involves β-catenin-mediated recruitment of HIPK2 to TCF3, culminating in dissociation of TCF3 from target gene promoters; TCF3 mutants resistant to Wnt-dependent phosphorylation act as constitutive repressors of Vent2 and Cdx4 during axis specification. Xenopus embryo phosphorylation assays, co-immunoprecipitation, ChIP, dominant-negative and phospho-resistant mutant analysis Developmental Cell High 20951344
2011 HIPK2 phosphorylates TCF3 (as well as LEF1 and TCF4) in response to Wnt8 stimulation in Xenopus embryos, causing dissociation of TCF3 from target promoters; upon HIPK2-mediated phosphorylation, TCF3 is replaced at target promoters by positively acting TCF1, revealing a TCF-switching mechanism for Wnt target gene activation. In vivo phosphorylation assays in Xenopus, ChIP, dominant-negative and kinase-dead HIPK2 constructs The Journal of Biological Chemistry High 21285352
2011 Tcf3 knockout ESCs show genome-wide increase in histone H3 acetylation (AcH3) and decrease in H3K9me3, establishing that Tcf3 repressor activity maintains heterochromatin marks; absence of Tcf3 dramatically enhances efficiency of somatic cell reprogramming by modifying the epigenome early in the process. Chromatin immunofluorescence, reprogramming efficiency assays, Tcf3 knockout ESCs PNAS Medium 21730189
2011 Tcf3 represses Wnt/β-catenin signaling in mouse neural stem cells and HEK293 cells by two independent mechanisms: competing with other Tcf/Lef family members for β-catenin binding, and competing for DNA binding at Wnt-responsive elements; simultaneous disruption of both mechanisms is required to fully relieve Tcf3 repressor activity; β-catenin/Tcf3 interaction occurs in the nucleus. Reporter assays, co-immunoprecipitation, immunofluorescence, N-terminal deletion mutant analysis Molecular and Cellular Biochemistry Medium 22270545
2011 Genetic ablation of Tcf3 in mice replaces the requirement for exogenous Wnt3a or GSK3 inhibition for ESC self-renewal, demonstrating that inhibition of Tcf3 repressor is the necessary downstream effect of Wnt signaling; Tcf3-β-catenin and Tcf1-β-catenin interactions both contribute to Wnt stimulation, and the combination of Tcf3 and Tcf1 recruits Wnt-stabilized β-catenin to Oct4 binding sites on ESC chromatin. Tcf3 genetic knockout, Wnt3a treatment, ChIP, ESC self-renewal assays Nature Cell Biology High 21685894
2011 In zebrafish embryos, Tcf3 suppresses cdx4 expression by direct binding to multiple sites in the cdx4 gene regulatory region; Tcf3 requires Groucho/TLE and HDAC1 corepressors for activity; the transcription factor E4f1 derepresses cdx4 by dissociating corepressors from Tcf3 without inhibiting its DNA binding; E3 ubiquitin ligase Lnx2b counteracts E4f1 effects. ChIP, reporter assays, co-immunoprecipitation, zebrafish embryo gain/loss-of-function The EMBO Journal High 21666599
2011 In the developing mouse neocortex, Tcf3 is expressed in undifferentiated neural progenitor cells (NPCs), functions as a repressor of Wnt signaling, binds to the Neurogenin1 promoter to repress its expression, and thereby inhibits neuronal differentiation while increasing NPC self-renewal; Wnt stimulation reduces Tcf3 levels and increases Tcf1 and Lef1, constituting a positive feedback loop that facilitates neuronal differentiation. Reporter gene assay, ChIP, gain/loss-of-function in primary NPCs, in vivo mouse analysis PLoS One Medium 24832538
2011 HESX1 and Tcf3 interact synergistically in a gene dosage-dependent manner to maintain anterior forebrain identity during mouse embryogenesis; Tcf3 is essential within neural ectoderm to maintain anterior character and repress Wnt/β-catenin targets; conditional deletion of β-catenin in the developing anterior forebrain of Hesx1-deficient embryos significantly rescues forebrain defects. Conditional knockout mouse genetics, zebrafish morpholino sensitized background, transcriptional profiling Development Medium 22007134
2012 Mouse embryos homozygous for a Tcf3ΔN knock-in mutation (ablating Tcf3-β-catenin interaction) progress through gastrulation without defect, genetically proving that Tcf3 function during gastrulation is β-catenin-independent; post-gastrulation defects in Tcf3ΔN/ΔN mice reveal that Tcf3-β-catenin indirectly activates target genes by relieving Tcf3 repression of Lef1, which then activates targets via Lef1-β-catenin complexes. Knock-in mouse genetics, epistasis analysis, in vivo developmental phenotyping Development High 22573616
2012 Esrrb is a pivotal target repressed by Tcf3 downstream of Gsk3 inhibition in ESCs; Esrrb knockdown/knockout eliminates response to Gsk3 inhibition; forced Esrrb expression phenocopies Gsk3 inhibition or Tcf3 deletion by suppressing differentiation and sustaining self-renewal, establishing Esrrb as necessary and sufficient to mediate self-renewal downstream of the Gsk3/Tcf3 axis. Genome localization analysis, transcriptome analysis, knockdown, knockout, forced expression assays in ESCs Cell Stem Cell High 23040478
2013 β-catenin inactivates Tcf7l1 (Tcf3) not by switching it to a coactivator complex but by removing it from DNA, which leads to Tcf7l1 protein degradation; mouse genetic experiments demonstrate that Tcf7l1 inactivation is the only required effect of the Tcf7l1-β-catenin interaction. Mouse genetics (knock-in alleles), ChIP, protein stability assays, breast cancer xenograft models Cell Reports High 23810553
2013 Tcf7l1 is necessary in pluripotent cells for lineage specification to occur concomitantly with gastrulation; in Tcf7l1−/− embryos, mesoderm specification is delayed and uncoupled from primitive streak induction; Tcf7l1 repressor activity enables a rapid switch in pluripotent cell response to Wnt/β-catenin from self-renewal to mesoderm specification. Tcf7l1 knockout mouse embryo analysis, conditional genetics, gene expression profiling Development High 23487311
2013 Wnt signaling down-regulates Tcf3 expression through decreased activating histone marks (H3K4me3, H3-acetylation) and upregulation of miR-211 (a novel Wnt-regulated microRNA targeting Tcf3); Tcf3 down-regulation is a primary response to Wnt activation (via APC mutation) and is necessary for Wnt-mediated suppression of neural differentiation in ESCs. ChIP-seq, miRNA overexpression, APC-mutant ESC lines with varying Wnt levels, rescue experiments PLoS Genetics Medium 23658527
2013 In granulosa cells, TCF3 is constitutively associated with the Lhcgr promoter; PKA-dependent phosphorylation of β-catenin on Ser552/Ser665 recruits it to the Lhcgr promoter together with SF1 upon FSH stimulation; dominant-negative TCF abolished FSH-induced Lhcgr reporter activity. Chromatin immunoprecipitation, adenoviral dominant-negative TCF, luciferase reporter assays, microarray Molecular Endocrinology Medium 23754802
2014 Tcf3 is upregulated in skin wounds; overexpression accelerates keratinocyte migration and wound healing; Stat3 is an upstream regulator of Tcf3; the pro-migration effects of Tcf3 are non-cell autonomous and β-catenin-independent; lipocalin-2 (LCN2) is the key secreted factor downstream of Tcf3 that promotes cell migration in vitro and wound healing in vivo. Gain/loss-of-function in keratinocytes and mouse wound healing models, pathway analysis, secretome studies Nature Communications High 24909826
2014 In zebrafish, in medaka, and in mammalian cells, Tcf3 repressor function depends critically on co-repressor interactions with Groucho/TLE proteins; inactivation of Groucho/Tle genes phenocopies tcf3 knockdown in anterior/eye development; Tcf3 function in eye development requires Groucho/Tle co-repressors. PNA-mediated knockdown in medaka, dominant-negative co-repressor approach, phenotypic analysis BMC Biotechnology Medium 29316906
2015 Jmjd6 interacts with Tcf7l1 at the region responsible for Groucho interaction, thereby displacing the Groucho transcriptional corepressor from Tcf7l1 and derepressing Tcf7l1 target genes; Jmjd6 antagonizes Tcf7l1-mediated repression and enhances β-catenin-induced gene activation; loss of Jmjd6 causes anteroposterior axis defects in Xenopus. Co-immunoprecipitation, reporter assays, Xenopus loss-of-function, competition binding The Journal of Biological Chemistry Medium 26157142
2015 Downstream of GSK3 inhibition, elevated cMyc and β-catenin act in parallel to reduce TCF7l1 levels: cMyc reduces Tcf7l1 mRNA, while β-catenin reduces Tcf7l1 DNA binding and promotes protein turnover; deletion of Tcf7l1 is sufficient to allow upregulation of FoxA2 (pioneer factor for endoderm) in the presence of Activin, identifying a cMyc/β-catenin-Tcf7l1-FoxA2 de-repression axis for endoderm induction. ESC differentiation assays, Tcf7l1 deletion, ChIP, epistasis experiments The EMBO Journal Medium 26675138
2015 TCF3 (Tcf7l1) binds the MYC 3' WRE to repress MYC in colorectal cancer cells; depletion of TCF3 increases availability of the MYC WRE to TCF4/β-catenin complexes; GSK3β inhibition causes an exchange of TCF3 with TCF4/β-catenin at the MYC WRE to activate MYC; this TCF factor switch controls MYC expression as quiescent cells re-enter the cell cycle. ChIP, shRNA knockdown, GSK3β inhibition, cell cycle analysis Cell Cycle Medium 25659031
2016 TCF7L1 loss in HCT116 colorectal cancer cells impaired growth and colony formation and reduced tumor growth in xenograft; TCF7L1 buffers CTNNB1/TCF target gene expression and its loss activates EPHB3 (a tumor suppressor); knockdown of EPHB3 partially restores growth of TCF7L1-null cells, demonstrating that TCF7L1 represses EPHB3 to promote CRC growth. TCF7L1 knockout in CRC cells, xenograft model, transcriptome analysis, epistasis via EPHB3 knockdown Scientific Reports Medium 27333864
2016 TCF7L1 promotes skin squamous cell carcinoma tumor growth, enhances cell migration, and overrides oncogenic RAS-induced senescence independently of its interaction with β-catenin; through transcriptome profiling and gain/loss-of-function studies, LCN2 was identified as a major downstream effector of TCF7L1 driving tumor growth. Separation-of-function mutants, β-catenin-interaction-deficient TCF7L1, mouse skin carcinogenesis model, xenograft, transcriptome profiling eLife High 28467300
2016 In human hypothalamo-pituitary (HP) axis development, TCF7L1 functions exclusively through its repressing activity (not β-catenin interaction) in the prospective hypothalamus to maintain hypothalamic signals needed for Rathke's pouch induction; two missense variants in human TCF7L1 (p.R92P, p.R400Q) found in patients with congenital hypopituitarism exhibit reduced repressing activity in vitro and in vivo. Conditional mouse knockout, human patient variant analysis, in vitro and in vivo repression assays PNAS High 26764381
2017 MEK inhibition suppresses LEF1 expression in mouse ESCs; knockdown/knockout of Lef1 partially mimics MEK inhibitor self-renewal effects; depletion of both Tcf3 and Lef1 enables maintenance of undifferentiated mouse ESCs without exogenous factors, demonstrating their combined role as differentiation drivers. Lef1 knockout/knockdown, MEK inhibition, transcriptome sequencing, ESC self-renewal assays Biology Open Medium 28288968
2019 TCF3 (Tcf7l1) sanctions rewiring of the naive ESC gene regulatory network by suppressing components of the ESC transcription factor circuitry; triple deletion of Etv5, Rbpj, and Tcf3 locks ESCs in self-renewal even under differentiation stimuli, demonstrating complementary roles for these three repressors as drivers of the naive-to-formative pluripotency transition. Triple gene deletion, genome-wide transcriptomics, ESC differentiation assays Cell Stem Cell High 31031137
2019 In liver cancer stem cells, Tcf7l1 suppresses self-renewal through transcriptional repression of the Nanog gene independently of β-catenin; IGF signaling stimulates Tcf7l1 phosphorylation and degradation through the MEK/ERK pathway, providing a mechanism by which extracellular signals modulate Tcf7l1 protein stability. Ectopic expression, shRNA knockdown, in vitro kinase/phosphorylation assays, tumor sphere assays Stem Cells Medium 31322782
2019 TCF7L1 in prostate cancer cells directly binds regulatory sequences of IL-8 and CXCR2 upon WNT4 activation to upregulate IL-8/CXCR2 signaling, driving neuroendocrine differentiation and cell motility; ADT-induced WNT4 secretion upregulates TCF7L1 in prostate cancer cells. ChIP, gene knockdown/overexpression, cytokine/receptor expression assays, prostate tissue analysis Oncogenesis Medium 34799554
2023 TCF7L1 transcriptional repression promotes primitive endoderm (PE) differentiation of mESCs and in the preimplantation inner cell mass; time-series RNA sequencing and ChIP data reveal that TCF7L1 binds and represses genes encoding naive pluripotency factors and regulators of formative pluripotency including Otx2 and Lef1; TCF7L1 deletion abrogates PE differentiation without restraining epiblast priming. RNA sequencing time-series, ChIP, Tcf7l1 conditional knockout, ESC lineage differentiation assays Nature Communications High 36869101
2024 Id2 binds Tcf3 through its HLH domain and disrupts assembly of the Tcf3-Tal1 transcriptional regulatory complex; this prevents Tcf3 interaction with histone demethylase LSD1, increasing permissive H3K4me2 at the Slamf6 promoter and epigenetically promoting generation of Slamf6+ progenitor exhausted CD8+ T cells; LSD1 inhibition rescues the Id2 knockout phenotype. Co-immunoprecipitation, ChIP-seq, ATAC-seq, Id2 knockout, LSD1 inhibitor treatment Cellular & Molecular Immunology High 38287103
2024 Motif analysis of enhancers in mouse oocytes and early embryos identified TCF3 and TCF12 as crucial regulators of oogenesis; deficiency of TCF3 (and TCF12) impairs activation of key oocyte genes and folliculogenesis in mice. H3K27ac CUT&TAG mapping, STARR-seq reporter assay, transcription factor motif analysis, TCF3 knockout mouse phenotyping Nature Cell Biology Medium 38839978
2014 5-carboxylcytosine (5caC) modification in the CG dinucleotide of the E-box motif (CGCAG|GTG) increases binding of the Tcf3|Ascl1 bHLH heterodimer approximately 10-fold, while not affecting other bHLH dimers tested with other cytosine modifications. In vitro DNA binding assays with modified oligonucleotide probes, systematic comparison of cytosine modifications Biochemical and Biophysical Research Communications Low 24835951

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2009 A census of human transcription factors: function, expression and evolution. Nature reviews. Genetics 1191 19274049
2017 Impact of cytosine methylation on DNA binding specificities of human transcription factors. Science (New York, N.Y.) 934 28473536
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2006 Hypoxia-inducible factor-1-dependent repression of E-cadherin in von Hippel-Lindau tumor suppressor-null renal cell carcinoma mediated by TCF3, ZFHX1A, and ZFHX1B. Cancer research 357 16510593
2000 Crystal structure of a beta-catenin/Tcf complex. Cell 353 11136974
2000 Repressor activity of Headless/Tcf3 is essential for vertebrate head formation. Nature 327 11057671
2012 Esrrb is a pivotal target of the Gsk3/Tcf3 axis regulating embryonic stem cell self-renewal. Cell stem cell 320 23040478
2001 All Tcf HMG box transcription factors interact with Groucho-related co-repressors. Nucleic acids research 310 11266540
2011 Opposing effects of Tcf3 and Tcf1 control Wnt stimulation of embryonic stem cell self-renewal. Nature cell biology 252 21685894
2006 Repression of Nanog gene transcription by Tcf3 limits embryonic stem cell self-renewal. Molecular and cellular biology 249 16894029
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