Affinage

GTF2I

General transcription factor II-I · UniProt P78347

Length
998 aa
Mass
112.4 kDa
Annotated
2026-06-10
100 papers in source corpus 46 papers cited in narrative 45 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GTF2I encodes TFII-I, a signal-responsive multifunctional transcription factor that defines an alternative, TFIID-dependent transcription initiation pathway by binding directly to initiator (Inr) elements at TATA-less promoters and cooperating with TBP to nucleate distinct preinitiation complexes (PMID:8377828). Through its tandem I-repeats and two separable DNA-binding regions, TFII-I recognizes both Inr and E-box elements and acts at basal and upstream regulatory sites of the same gene, often synergizing with partner factors such as USF1 (PMID:9384587, PMID:11113127, PMID:15941713). It integrates growth-factor and stress signaling at immediate-early and signal-induced promoters—most extensively the c-fos SRE/SIE, which it activates in complex with SRF, Phox1, STAT1/STAT3 and the Ras/MAPK pathway (PMID:9334314, PMID:9584171). Its activity is gated by an unusually dense post-translational network: cytoplasmic-to-nuclear shuttling and transactivation are driven by tyrosine phosphorylation from Btk, Itk, JAK2 and c-Src at residues including Y248, Y357, Y462 and Y611, and by serine phosphorylation from ERK (S627/S633), PKG Iβ (S371/S743) and Cdk1, while Btk and the related repressor MusTRD1/BEN tether or exclude it from the nucleus (PMID:10373551, PMID:10648599, PMID:11313464, PMID:11373296, PMID:12082086, PMID:11934902, PMID:14623887, PMID:19701889, PMID:11438732). TFII-I transcriptional output is further tuned by HDAC3-mediated repression, which is relieved by PIASxβ and by PIAS4-driven SUMOylation at K221/K240 that weakens HDAC3 binding, and the protein is targeted for p53/ATM-dependent ubiquitin–proteasomal degradation upon genotoxic stress (PMID:12393887, PMID:12239342, PMID:25869096, PMID:16314517). Beyond core promoter control, TFII-I links to broad genome organization and signaling: it partners with CTCF to direct promoter-proximal CTCF occupancy and Pol II Ser5 phosphorylation at metabolic genes, mediates Igh enhancer–promoter looping with OCA-B, transduces TGFβ signals via Smad2/3, mediates the ER stress response as the ERSE-binding factor acting with ATF6, drives cyclin D1-dependent S-phase progression, and supports translesion DNA synthesis by bridging PCNA and Pol ζ via Rev7 (PMID:25646466, PMID:21549311, PMID:16055724, PMID:11287625, PMID:16314517, PMID:19182516, PMID:24922507). Outside the nucleus, TFII-I suppresses agonist-induced calcium entry by competing with TRPC3 for PLCγ binding (PMID:17023658). Haploinsufficiency and dosage imbalance of GTF2I underlie Williams-Beuren syndrome neurocognitive and myelination phenotypes, acting in part through an LSD1-dependent program controlling neural progenitor proliferation and oligodendrocyte maturation, while the recurrent L424H mutation drives thymic epithelial transformation through COX-2 and metabolic gene upregulation (PMID:31011227, PMID:38019906, PMID:32034314, PMID:36049655).

Mechanistic history

Synthesis pass · year-by-year structured walk · 32 steps
  1. 1993 High

    Established that TFII-I is not merely an accessory factor but defines a distinct initiation pathway, answering how TATA-less, Inr-containing promoters recruit the basal machinery.

    Evidence In vitro transcription reconstitution and preinitiation complex assembly with defined factors

    PMID:8377828

    Open questions at the time
    • Did not identify physiological target promoters in vivo
    • Structural basis of Inr recognition undefined
  2. 1993 High

    Showed the TFII-I initiation pathway is a regulatable node by demonstrating Myc selectively blocks TFII-I-dependent (not TFIIA-dependent) preinitiation, framing TFII-I as a target of oncogenic control.

    Evidence In vitro transcription and PIC formation assays with co-IP

    PMID:8377829

    Open questions at the time
    • Physiological promoters subject to Myc–TFII-I antagonism not defined
    • In vivo relevance not tested
  3. 1997 High

    Defined TFII-I primary structure (six I-repeats) and dual Inr/E-box DNA-binding capacity, and connected it to upstream factors (USF1, SRF, Phox1) at serum-responsive promoters, explaining how one protein bridges core and enhancer elements.

    Evidence cDNA cloning, domain analysis, DNA-binding and reporter assays, biochemical purification (as SPIN)

    PMID:9334314 PMID:9384587

    Open questions at the time
    • Mechanism of E-box vs Inr selectivity unresolved
    • No structural model of I-repeats
  4. 1997 High

    Linked TFII-I to receptor signaling by identifying it as a Btk-associated Btk substrate phosphorylated upon BCR crosslinking, opening the kinase-regulated dimension of its biology.

    Evidence Co-IP, in vitro kinase assay, PH-domain binding mapping, BCR crosslinking

    PMID:9012831

    Open questions at the time
    • Functional consequence of phosphorylation not yet shown
    • Which tyrosines phosphorylated not mapped here
  5. 1998 Medium

    Showed Inr-specific transcriptional function resides in the N-terminal DNA-binding domain and that tyrosine phosphorylation modulates transactivation without affecting DNA binding, separating recruitment from activation.

    Evidence Dominant-negative truncation mutants, in vivo phosphorylation labeling, reporter assays on the TCR Vβ promoter

    PMID:9671454 PMID:9837922

    Open questions at the time
    • Single-lab functional dissection
    • Specific kinases for basal phosphorylation not identified
  6. 1999 High

    Defined the cytoplasm–nucleus shuttling logic: Btk tethers TFII-I in the cytoplasm and BCR signaling dissociates the complex to permit nuclear import, establishing signal-gated subcellular localization.

    Evidence Co-IP with Btk domain mutants, subcellular fractionation, BCR crosslinking, reporter assays

    PMID:10373551

    Open questions at the time
    • Import receptor / NLS machinery not defined
    • Quantitative kinetics of shuttling unknown
  7. 2000 Medium

    Resolved the structural determinants of oligomerization and DNA binding, showing self-association via the N-terminal leucine zipper and I-repeats aids nuclear translocation and tunes basal vs signal-responsive output.

    Evidence Deletion/point mutagenesis, co-IP, fractionation, reporter assays

    PMID:10854432 PMID:11113127

    Open questions at the time
    • Stoichiometry of homo/heteromers undefined
    • Isoform-specific roles incompletely mapped
  8. 2000 High

    Connected TFII-I to MAPK signaling mechanistically by mapping an ERK docking D-box and ERK phosphorylation sites (S627/S633) required for c-fos activation.

    Evidence Co-IP, in vitro kinase assay, point mutagenesis, dominant-negative Ras, reporter assays

    PMID:10648599

    Open questions at the time
    • How serine phosphorylation alters complex assembly not detailed
  9. 2001 High

    Identified TFII-I as the ER stress response element-binding factor (ERSF) acting with ATF6, extending its role to the unfolded protein response at grp78/ERp72 promoters.

    Evidence Chromatographic purification, microsequencing, recombinant binding, co-IP with ATF6, knockdown, reporter assays

    PMID:11287625

    Open questions at the time
    • How ER stress signal reaches TFII-I not defined here
  10. 2001 High

    Mapped specific tyrosine kinases (JAK2 at Y248; Btk at Y248/Y357/Y462) to defined residues required for c-fos activity, dissecting which inputs converge on which sites.

    Evidence In vitro kinase assays, phosphopeptide mapping, site-directed mutagenesis, dominant-negative JAK2, reporter assays

    PMID:11313464 PMID:11373296

    Open questions at the time
    • Combinatorial logic of multi-site phosphorylation untested
    • Spatial/temporal ordering of kinase action unknown
  11. 2001 Medium

    Showed the TFII-I-related repressor MusTRD1/BEN antagonizes TFII-I by NLS-dependent nuclear exclusion, identifying a paralog-based regulatory switch.

    Evidence Co-expression, localization microscopy, fractionation, NLS mutagenesis, reporter assays

    PMID:11438732

    Open questions at the time
    • Single-lab study
    • In vivo physiological context of antagonism not established
  12. 2002 High

    Established the repressive arm of TFII-I regulation by identifying HDAC3 as a bound deacetylase that suppresses transactivation, and PIASxβ/SUMO pathway as a relieving counterforce.

    Evidence Immunoaffinity purification, co-IP, GST pulldown, HDAC activity assay, reporter assays

    PMID:12193603 PMID:12239342 PMID:12393887

    Open questions at the time
    • Direct demonstration that SUMOylation displaces HDAC3 came later
    • Genome-wide target promoters of repression not mapped
  13. 2002 High

    Extended kinase regulation to serine/threonine and second-messenger pathways by mapping PKG Iβ phosphorylation at S371/S743 and c-Src phosphorylation at Y248/Y611 driving nuclear translocation.

    Evidence Yeast two-hybrid, in vitro kinase assays, mutagenesis, fractionation, stable c-fos reporter cells

    PMID:11934902 PMID:12082086

    Open questions at the time
    • Crosstalk between Ser and Tyr modifications not integrated
    • Stoichiometry in vivo unknown
  14. 2003 Medium

    Clarified that Btk and Src target distinct sites and that Btk tethers TFII-I cytoplasmically by preventing dimerization, showing parallel kinase pathways converge with opposing localization outcomes.

    Evidence Domain mapping with deletion/point mutants, co-IP, fractionation

    PMID:14623887

    Open questions at the time
    • Single-lab domain study
    • Whether dimerization-coupled import is direct mechanism untested structurally
  15. 2005 High

    Defined TFII-I as a signal-recruited Smad partner in TGFβ/activin signaling controlling developmental and cell-cycle genes, with Ser371/S743 phosphorylation tuning Smad complex formation.

    Evidence Co-IP, ChIP, siRNA knockdown, Xenopus antisense, microarray, reporter assays

    PMID:16055503 PMID:16055724

    Open questions at the time
    • Direct vs cofactor-mediated DNA contact at Gsc DE not resolved
    • How phosphorylation alters Smad affinity mechanistically unclear
  16. 2005 Medium

    Demonstrated dual Inr/E-box action on endogenous promoters (VEGFR-2) and that c-Src phosphorylation at Y248 couples ER stress to Grp78 induction, unifying its DNA-binding versatility with signal input.

    Evidence Gel shift, siRNA, reporter/mutagenesis, ChIP, phospho-specific antibodies, stable knockdown

    PMID:15664986 PMID:15941713

    Open questions at the time
    • Counter-regulation by TFII-IRD1 mechanism incomplete
    • Generality across other Inr/E-box genes untested
  17. 2006 High

    Revealed a non-transcriptional cytoplasmic function: TFII-I suppresses agonist-induced calcium entry by competing with TRPC3 for PLCγ binding, expanding its role beyond the nucleus.

    Evidence Calcium entry assays, TRPC3 surface expression, PLCγ SH2/PH-domain interaction mapping

    PMID:17023658

    Open questions at the time
    • In vivo physiological calcium contexts not established
    • Reciprocal regulation of nuclear vs cytoplasmic pools unclear
  18. 2006 Medium

    Connected TFII-I to immunoglobulin gene regulation in B cells through ARID3a/Bright interaction and tyrosine-dependent heavy-chain transcription.

    Evidence Co-IP, siRNA knockdown, reporter assays, mutagenesis

    PMID:16738337

    Open questions at the time
    • Single-lab study
    • Mechanism of looping not yet shown (later defined via OCA-B)
  19. 2007 Medium

    Established a role in B-cell growth control, with TFII-I restraining c-Myc and modulating NF-κB and CDK inhibitors during signal-dependent growth arrest.

    Evidence shRNA silencing, immunoblotting, EMSA for NF-κB subunits, proliferation/apoptosis assays

    PMID:17312101

    Open questions at the time
    • Direct vs indirect transcriptional effects on c-Myc/NF-κB not separated
    • Single-lab data
  20. 2007 Medium

    Showed TFII-I cooperates with USF1/USF2 to reactivate latent integrated HIV-1 via the LTR RBEIII element in a TCR/MAPK-dependent manner, extending its enhancer cooperativity to viral transcription.

    Evidence EMSA, ChIP, dominant-interfering constructs, TCR crosslinking, MEK inhibition

    PMID:15767439 PMID:17546494

    Open questions at the time
    • Quantitative contribution to latency reversal in primary cells not assessed
  21. 2008 Medium

    Implicated TFII-I in dyslexia-associated regulatory variation by showing allele-specific binding within a PARP1/SFPQ complex at the DYX1C1 promoter SNP.

    Evidence EMSA, MS identification, protein sequencing, luciferase reporter assays

    PMID:18445785

    Open questions at the time
    • Causal link to dyslexia phenotype not established
    • Functional role of PARP1/SFPQ partnership undefined
  22. 2008 Medium

    Extended TFII-I function to transcription elongation by demonstrating Elongin A interaction and Pol II/Elongin A-coupled recruitment at the stress-responsive ATF3 gene genome-wide.

    Evidence Biotinylation-tagging ChIP-seq, pulldown, siRNA, Pol II/Elongin A ChIP

    PMID:24875474

    Open questions at the time
    • Direct mechanistic role in elongation vs recruitment not resolved
    • Single-lab genome-wide dataset
  23. 2009 High

    Defined TFII-I as a cell-cycle regulator: it activates cyclin D1 to promote S-phase progression, is degraded by p53/ATM-dependent ubiquitination upon genotoxic stress, and is phosphorylated by Cdk1 at the G2/M boundary.

    Evidence ChIP, ubiquitination/proteasome assays, stable cells, flow cytometry, mutagenesis, microarray

    PMID:16314517 PMID:19182516

    Open questions at the time
    • E3 ligase mediating p53-dependent degradation not identified
    • Direct Cdk1 site on TFII-I not mapped here
  24. 2009 Medium

    Identified Itk as an additional T-cell tyrosine kinase phosphorylating TFII-I downstream of TCR engagement to potentiate c-fos transcription.

    Evidence Co-IP, TCR-crosslinking phosphorylation, kinase-dead/R29C mutants, reporter assays, deletion mapping

    PMID:19701889

    Open questions at the time
    • Itk target tyrosines not mapped
    • Redundancy with Btk in B vs T cells unresolved
  25. 2011 High

    Provided a 3D chromatin mechanism for Igh regulation: promoter-bound TFII-I and enhancer-bound OCA-B mediate enhancer–promoter looping, with OCA-B relieving HDAC3 repression by competing for TFII-I.

    Evidence Co-IP, ChIP, chromosome conformation capture, competition binding, reporter assays

    PMID:21549311

    Open questions at the time
    • Generality of TFII-I-mediated looping at other loci untested
  26. 2014 Medium

    Revealed a transcription-independent genome-maintenance role: TFII-I bridges PCNA and Pol ζ via Rev7 to support translesion synthesis and DNA damage tolerance.

    Evidence Co-IP, TLS functional assays, homodimerization and PCNA-binding mutants

    PMID:24922507

    Open questions at the time
    • Structural basis of the PCNA–Pol ζ bridge undefined
    • Single-lab study
  27. 2015 High

    Placed TFII-I in genome organization by showing it directs CTCF promoter-proximal occupancy and Pol II Ser5 phosphorylation at metabolic genes, and refined its PTM logic by defining PIAS4-mediated SUMOylation at K221/K240 that antagonizes HDAC3 binding.

    Evidence MS of CTCF interactors, fractionation, ChIP-seq, siRNA; SUMO site mapping, mutagenesis, proliferation/colony assays

    PMID:25646466 PMID:25869096

    Open questions at the time
    • Whether TFII-I recruits or stabilizes CTCF mechanistically unclear
    • Link between SUMO and CTCF arms not integrated
  28. 2016 Medium

    Showed viral exploitation of TFII-I turnover: adenovirus E4-ORF3 first stimulates SUMOylation then drives ubiquitin–proteasomal degradation of TFII-I to derepress a viral promoter.

    Evidence Co-IP, ubiquitination/proteasome assays, reporter assays, infection

    PMID:26814176

    Open questions at the time
    • E3 ligase for E4-ORF3-induced degradation not identified
    • Single virus context
  29. 2019 High

    Established a causal neurodevelopmental mechanism for Williams-Beuren features: neuronal Gtf2i loss reduces oligodendrocyte maturation and myelination, with deficits rescued pharmacologically.

    Evidence Neuron-specific conditional knockout, mRNA-seq, EM myelin imaging, electrophysiology, clemastine rescue

    PMID:31011227

    Open questions at the time
    • Direct transcriptional targets driving myelination program not pinpointed
    • Cell-autonomous vs non-autonomous signal to oligodendrocytes unresolved
  30. 2023 High

    Defined the dosage-sensitive neurodevelopmental program and effector: GTF2I controls cortical progenitor proliferation and neuron differentiation through LSD1, with LSD1 inhibition rescuing duplication-driven phenotypes.

    Evidence Patient-derived cortical organoids, scRNA-seq, proteomics, transgenic mice, LSD1 inhibitor, behavioral assays

    PMID:38019906

    Open questions at the time
    • Direct biochemical GTF2I–LSD1 mechanism at chromatin not fully mapped
    • Generalizability across patient genetic backgrounds untested
  31. 2020 Medium

    Identified the oncogenic mechanism of the recurrent L424H mutation in thymic epithelium: mutant TFII-I upregulates COX-2 and glycolytic genes required for transformation and survival under metabolic stress.

    Evidence L424H knock-in cells, transcriptomics, transformation assays, COX-2 inhibition, metabolic stress assays

    PMID:32034314

    Open questions at the time
    • How L424H alters DNA binding/specificity not defined
    • Single-lab cellular model
  32. 2022 Medium

    Confirmed L424H as an in vivo thymic oncogenic driver, impairing medullary thymic epithelial maturation and driving E2F/MYC-associated thymoma in aged mice.

    Evidence Conditional Foxn1-driven knock-in mouse, spatial transcriptomics, IHC, TCR repertoire analysis

    PMID:36049655

    Open questions at the time
    • Mechanistic link from L424H to E2F/MYC signature not dissected
    • Long latency mechanism unexplained

Open questions

Synthesis pass · forward-looking unresolved questions
  • How TFII-I integrates its dense multi-kinase, SUMO, ubiquitin, and acetylation inputs into a unified code that selects among its many DNA-binding, looping, calcium-suppressing, and DNA-repair functions remains unresolved at the structural and quantitative level.
  • No high-resolution structure of full-length TFII-I or its I-repeat DNA complexes
  • Combinatorial PTM logic governing function selection undefined
  • Mechanism by which L424H rewires specificity toward oncogenic programs unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 8 GO:0003677 DNA binding 4 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 1 GO:0140223 general transcription initiation factor activity 1
Localization
GO:0005634 nucleus 5 GO:0005654 nucleoplasm 3 GO:0005829 cytosol 3
Pathway
R-HSA-74160 Gene expression (Transcription) 5 R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 4 R-HSA-1643685 Disease 3 R-HSA-1266738 Developmental Biology 2 R-HSA-1640170 Cell Cycle 2 R-HSA-4839726 Chromatin organization 2 R-HSA-8953897 Cellular responses to stimuli 2 R-HSA-73894 DNA Repair 1
Partners
ATF6BTKCTCFERK/MAPK1HDAC3JAK2SMAD2SRC
Complex memberships
TFII-I/CTCF chromatin complexTFII-I/OCA-B Igh looping complexTFII-I/PARP1/SFPQ complexTFII-I/Smad2/3 complex

Evidence

Reading pass · 45 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 TFII-I defines an alternative transcription initiation pathway through direct binding to the initiator (Inr) element, forming preinitiation complexes distinct from those formed with TFIIA; TBP binds cooperatively with TFII-I at Inr-containing TATA-less promoters, enabling a TFIID-dependent pathway at TATA-less promoters. In vitro transcription reconstitution, preinitiation complex assembly assays, sequential factor addition Nature High 8377828
1993 Myc interacts physically with TFII-I and inhibits TFII-I-dependent transcription initiation selectively, correlating with prevention of TBP–TFII-I–promoter complex formation; this inhibition is specific to the TFII-I-dependent (not TFIIA-dependent) initiation pathway. In vitro transcription assay, protein–protein interaction (co-immunoprecipitation/pulldown), preinitiation complex formation assays Nature High 8377829
1997 TFII-I encodes a 120 kDa polypeptide containing six directly repeated ~90-residue I-repeat motifs each with a helix-loop/span-helix structure; recombinant TFII-I binds independently to both Inr and E-box elements, and acts synergistically with USF1 to activate transcription in vivo through both elements of the adenovirus major late promoter. cDNA cloning, ectopic expression, DNA-binding assays, in vivo transcription reporter assays, domain analysis of USF1 The EMBO journal High 9384587
1997 TFII-I (identified as SPIN) interacts with serum response factor (SRF) and Phox1 in vitro and in vivo, promotes formation of stable higher-order SRF/Phox1/DNA complexes, and binds multiple sequences in the c-fos promoter to cooperate with Phox1 for serum-inducible transcription through the c-fos SRE. Protein purification, molecular cloning, in vitro binding assays, co-immunoprecipitation, cotransfection reporter assays Genes & development High 9334314
1997 BAP-135 (TFII-I/GTF2I) is associated with Bruton's tyrosine kinase (Btk) in B cells via the Btk pleckstrin homology (PH) domain; it is a direct substrate for Btk-mediated tyrosine phosphorylation and is transiently phosphorylated on tyrosine following BCR crosslinking. Co-immunoprecipitation, in vitro kinase assay, PH domain binding mapping, BCR crosslinking experiment Proceedings of the National Academy of Sciences of the United States of America High 9012831
1998 TFII-I is required for efficient expression of the TATA-less, Inr-containing murine T-cell receptor Vβ5.2 promoter in vivo; an N-terminal protease-resistant DNA-binding fragment (p70) acts as a dominant negative inhibitor of Inr-specific function, demonstrating that the Inr-specific transcriptional function of TFII-I is dictated by its N-terminal domain and not its C-terminal activation domain. Transient transfection reporter assays, dominant-negative mutant analysis, ectopic expression of N-terminal fragment Molecular and cellular biology Medium 9671454
1998 TFII-I is phosphorylated in vivo on both serine/threonine and tyrosine residues basally; mutation of a consensus tyrosine phosphorylation site severely reduces TFII-I-mediated basal transcriptional activation of the Vβ promoter in vivo, while phosphorylation does not affect DNA binding. In vivo phosphorylation assays (metabolic labeling), site-directed mutagenesis, transcription reporter assays The Journal of biological chemistry Medium 9837922
1998 TFII-I enhances c-fos promoter activation through binding to the SIE and SRE upstream elements; it forms in vivo protein–protein complexes with SRF, STAT1, and STAT3; growth factor stimulation enhances tyrosine phosphorylation of TFII-I; and the Ras/MAPK pathway is required for TFII-I activity on the c-fos promoter. Co-immunoprecipitation, transient transfection reporter assays, site-directed mutagenesis, in vivo tyrosine phosphorylation assay Molecular and cellular biology Medium 9584171
1999 TFII-I constitutively associates with wild-type and kinase-inactive Btk but not xid Btk (R28C PH domain mutation) in vivo; Btk's kinase domain is required to enhance TFII-I tyrosine phosphorylation and transcriptional activity; BCR crosslinking causes dissociation of TFII-I from Btk and increased nuclear import of TFII-I in wild-type but not xid B cells. Co-immunoprecipitation, transient transfection reporter assays, nuclear/cytoplasmic fractionation, BCR crosslinking Molecular and cellular biology High 10373551
2000 TFII-I forms stable homo- and heteromeric complexes via both its N-terminal region (containing a leucine zipper-like motif) and its I-repeats; complex formation aids nuclear translocation of TFII-I; co-expression of different isoforms leads to enhanced basal but attenuated signal-responsive transcriptional activity. Co-immunoprecipitation, nuclear/cytoplasmic fractionation, isoform-specific antibodies, reporter transcription assays The Journal of biological chemistry Medium 10854432
2000 TFII-I has two distinct DNA-binding regions; deletion of either abolishes DNA binding and transcriptional activation; I-repeats mediate homomeric interactions individually or in combination; an additional homomeric interaction domain resides within the N-terminal leucine zipper region. Deletion mutagenesis, DNA-binding assays, transcription reporter assays, protein–protein interaction assays The Journal of biological chemistry Medium 11113127
2000 ERK forms an in vivo complex with TFII-I through a consensus MAP kinase interaction domain (D-box) in TFII-I; ERK phosphorylates TFII-I in vitro at Ser627 and Ser633; mutation of the D-box or the ERK phosphorylation sites impairs TFII-I binding to ERK and its ability to enhance the c-fos promoter; serum stimulation enhances TFII-I–ERK complex formation. Co-immunoprecipitation, in vitro kinase assay, point mutagenesis, dominant-negative Ras, reporter assays Molecular and cellular biology High 10648599
2001 TFII-I is identified as the ERSE-binding factor (ERSF) that binds the ER stress response element (ERSE) in the grp78 and ERp72 promoters; purified recombinant TFII-I isoforms bind directly to ERSEs; ER stress (thapsigargin) increases TFII-I transcript and protein levels in the nucleus; TFII-I tyrosine phosphorylation sites are required for its activation of the Grp78 promoter; TFII-I physically interacts with ATF6 and is required for optimal ATF6-mediated ERSE stimulation. Chromatographic purification, protein microsequencing, recombinant protein binding assays, co-immunoprecipitation, reporter assays, stable knockdown Molecular and cellular biology High 11287625
2001 JAK2 phosphorylates TFII-I at Tyr248 in vivo and in vitro; this phosphorylation event is required for TFII-I interaction with ERK and for TFII-I activity on the c-fos promoter; dominant-negative JAK2 or JAK2 inhibitor AG490 abolishes TFII-I activity on c-fos. In vitro kinase assay, co-immunoprecipitation, site-directed mutagenesis (Y248F), dominant-negative JAK2 expression, reporter assays Molecular and cellular biology High 11313464
2001 Btk phosphorylates BAP/TFII-I predominantly at Tyr248, Tyr357, and Tyr462 in vitro and in vivo; mutation of any single site reduces c-fos promoter transcription, consistent with phosphorylation at these sites contributing to transcriptional activation. Site-directed mutagenesis, phosphopeptide mapping, in vitro kinase assay, co-expression with Btk in mammalian cells, reporter assays The Journal of biological chemistry High 11373296
2002 HDAC3 copurifies with TFII-I in immunoaffinity purification, co-immunoprecipitates with TFII-I, and colocalizes with it; the HDAC3–TFII-I interaction requires the C-terminal region of HDAC3 (residues 373–401) and residues 363–606 of TFII-I; an anti-TFII-I immunoprecipitate contains HDAC3 enzymatic activity; overexpression of HDAC3 severely reduces TFII-I transcriptional activation. Immunoaffinity purification, co-immunoprecipitation, GST pull-down, indirect immunofluorescence colocalization, HDAC enzymatic activity assay, deletion mutagenesis The Journal of biological chemistry High 12393887
2002 TFII-I and HDAC3 physically and functionally interact; PIASxβ (an E3 SUMO ligase) interacts with both TFII-I and HDAC3, relieves HDAC3-mediated repression of TFII-I transcriptional activation, suggesting SUMO pathway cross-talk with histone deacetylation at TFII-I target promoters. Co-immunoprecipitation, subcellular colocalization, transcription reporter assays Proceedings of the National Academy of Sciences of the United States of America Medium 12239342
2002 cGMP-dependent protein kinase Iβ (PKG Iβ) physically interacts with TFII-I via the N-terminal 93 amino acids of PKG Iβ and one of the six I-repeats of TFII-I; PKG phosphorylates TFII-I in vitro and in vivo at Ser371 and Ser743; mutation of these sites abolishes PKG-mediated enhancement of TFII-I transactivation of an SRE-containing promoter. Yeast two-hybrid screen, in vitro binding with purified recombinant proteins, co-immunoprecipitation, in vitro kinase assay, site-directed mutagenesis, reporter assays The Journal of biological chemistry High 12082086
2002 PIASxβ/Miz1 (SUMO E3 ligase) interacts with TFII-I and with hMusTRD1/BEN; ectopic PIASxβ augments TFII-I transcriptional activity and relieves BEN-mediated repression; nuclear-localization-deficient PIASxβ fails to alter TFII-I subcellular localization. Yeast two-hybrid screen, co-immunoprecipitation in mammalian cells, reporter transcription assays, localization studies The Journal of biological chemistry Medium 12193603
2002 c-Src phosphorylates TFII-I at Tyr248 and Tyr611 in a growth-factor-dependent manner; phosphorylated TFII-I translocates to the nucleus where it activates a stably integrated c-fos reporter; phosphorylation-deficient mutants (Y248F, Y611F) fail to activate the c-fos promoter; signal withdrawal leads to loss of nuclear TFII-I. In vivo tyrosine phosphorylation assays, site-directed mutagenesis, nuclear/cytoplasmic fractionation, stable c-fos reporter cell lines The Journal of biological chemistry High 11934902
2001 The TFII-I-related factor MusTRD1/BEN represses TFII-I transcriptional activity by excluding TFII-I from the nucleus when co-expressed; mutation of a nuclear localization signal in MusTRD1/BEN reverses this nuclear exclusion and restores c-fos promoter activity. Ectopic co-expression, subcellular localization (fluorescence microscopy), nuclear/cytoplasmic fractionation, reporter assays, NLS mutagenesis Proceedings of the National Academy of Sciences of the United States of America Medium 11438732
2003 The N-terminal ~90-amino acid region of TFII-I (including a leucine zipper motif) is primarily responsible for its physical interaction with Btk; Btk tethers TFII-I to the cytoplasm by preventing dimerization and nuclear localization; Src-dependent TFII-I tyrosine phosphorylation sites are distinct from those targeted by Btk, indicating two independent kinase pathways converge on TFII-I. Structural analysis with TFII-I deletion/point mutants, co-immunoprecipitation, nuclear/cytoplasmic fractionation The Journal of biological chemistry Medium 14623887
2005 TFII-I forms a complex with Smad2 upon TGFβ/activin stimulation, is recruited to the distal element (DE) of the goosecoid (Gsc) promoter, and activates Gsc transcription; siRNA knockdown of TFII-I abolishes TGFβ-mediated Gsc induction; in Xenopus, antisense knockdown of TFII-I decreases Gsc expression; BEN constitutively occupies the DE in the absence of TGFβ and is replaced by the TFII-I/Smad2 complex upon stimulation. Co-immunoprecipitation, chromatin immunoprecipitation, siRNA knockdown, reporter assays, Xenopus antisense experiments Molecular and cellular biology High 16055724
2005 TGFβ1 stimulates TFII-I phosphorylation at Ser371 and Ser743; mutation of these sites (S371A/S743A) enhances complex formation between TFII-I and Smad3 and increases their cooperative transcriptional regulation of cyclin D2, cyclin D3, and E2F2 genes. Phosphoproteome profiling, site-directed mutagenesis, co-immunoprecipitation, microarray expression analysis, luciferase reporter assay Molecular biology of the cell Medium 16055503
2005 TFII-I is phosphorylated at Tyr248 by c-Src in response to thapsigargin (ER stress); c-Src activation by ER stress stimulates Grp78 promoter activity via TFII-I; stable cells with suppressed TFII-I levels show reduced Grp78 induction; ChIP demonstrates enhanced TFII-I binding to the Grp78 promoter upon ER stress. In vivo phosphorylation assays (phospho-specific antibodies), stable TFII-I knockdown, chromatin immunoprecipitation, reporter assays The Journal of biological chemistry High 15664986
2005 TFII-I binds the VEGFR-2/KDR Inr element and three regulatory E-boxes in the VEGFR-2 promoter; siRNA-mediated reduction of TFII-I decreases endogenous VEGFR-2 expression; TFII-I can act at both basal Inr and upstream regulatory sites of the same promoter; TFII-IRD1 counter-regulates the same promoter. Gel shift assays, siRNA knockdown, reporter assays, mutagenesis of Inr and E-boxes The Journal of biological chemistry Medium 15941713
2005 PKG Iβ interaction with TFII-I requires a cluster of acidic amino acids in the PKG Iβ N-terminal leucine zipper (D26/E31); mutation D26K/E31R abrogates binding to TFII-I; basic residues in TFII-I within a putative α-helical region mediate binding to PKG Iβ. Site-directed mutagenesis, in vitro binding assays with purified proteins, co-immunoprecipitation in intact cells The Journal of biological chemistry Medium 16166082
2006 TFII-I acts outside the nucleus as a negative regulator of agonist-induced calcium entry (ACE) by suppressing surface accumulation of TRPC3 channels; this inhibition requires phosphotyrosine residues that engage SH2 domains of PLCγ and a PH-like domain of TFII-I that binds the split PH domain of PLCγ, suggesting TFII-I competes with TRPC3 for PLCγ binding. Calcium entry assays, surface expression of TRPC3, domain mapping, phosphotyrosine-dependent interaction assays with PLCγ SH2 domains Science High 17023658
2006 TFII-I directly interacts with Bright/ARID3a through Bright's protein interaction domain; specific tyrosine residues of TFII-I are essential for Bright-induced immunoglobulin reporter gene activity; TFII-I knockdown in B cells reduces heavy-chain transcript levels. Co-immunoprecipitation, siRNA knockdown, reporter assays, site-directed mutagenesis Molecular and cellular biology Medium 16738337
2007 TFII-I promotes B cell growth arrest in a signal-dependent manner by controlling c-Myc transcription and regulating NF-κB; loss of TFII-I function leads to up-regulation of c-Myc and down-regulation of p21 and p27, as well as increased nuclear c-rel and decreased p50 NF-κB DNA-binding activity. Stable post-transcriptional silencing (shRNA), immunoblotting, EMSA for NF-κB subunits, cell proliferation/apoptosis assays Journal of immunology Medium 17312101
2007 USF1, USF2, and TFII-I bind cooperatively to the HIV-1 LTR RBEIII element and are required for induction of latent integrated HIV-1 in response to T-cell receptor signaling; TFII-I stimulates USF1/USF2 binding to RBEIII ~160-fold less efficiently without TFII-I; dominant-interfering TFII-I inhibits induction; MAPK pathway is essential for induction. Electrophoretic mobility shift assay, chromatin immunoprecipitation, dominant-interfering constructs, T-cell receptor crosslinking, MEK inhibitor treatment Virus genes Medium 15767439 17546494
2008 TFII-I forms a complex with PARP1 and SFPQ that binds to the DYX1C1 promoter SNP rs3743205; electrophoretic mobility shift assays show allele-specific TFII-I binding; luciferase assays show allelic differences in DYX1C1 promoter activity linked to the TFII-I binding site. Electrophoretic mobility shift assay, mass spectrometry identification of protein complex, protein sequencing, luciferase reporter assays FASEB journal Medium 18445785
2009 TFII-I is recruited to the cyclin D1 promoter under normal growth conditions and transcriptionally activates it; upon genotoxic stress and p53 activation, TFII-I is ubiquitinated and degraded by the proteasome in a p53- and ATM-dependent manner; stable TFII-I expression increases cyclin D1 levels, accelerates S-phase entry/exit, and overcomes p53-mediated cell cycle arrest; these effects require tyrosine phosphorylation at Tyr248 and Tyr611. Chromatin immunoprecipitation, ubiquitination assays, proteasome inhibitor experiments, stable cell lines, flow cytometry, site-directed mutagenesis Molecular and cellular biology High 16314517
2009 TFII-I silencing causes unexpected defects in S-phase progression (delay entering and executing S-phase and entry into G2/M); microarray and functional validation identify cyclin D1 and PKC-β as major downstream transcriptional targets; Cdk1 phosphorylates TFII-I at the G2/M boundary, likely displacing it from condensed chromatin. siRNA knockdown, flow cytometry (cell cycle analysis), microarray, functional validation assays, Cdk1 phosphorylation assay Cell cycle Medium 19182516
2009 Inducible tyrosine kinase (Itk) physically interacts with TFII-I in T cells; Itk phosphorylates TFII-I upon T-cell receptor crosslinking; kinase-dead or R29C mutant Itk fails to phosphorylate TFII-I; Itk potentiates TFII-I-driven c-fos transcription; the first 90 N-terminal residues of TFII-I are dispensable for Itk binding. Co-immunoprecipitation, phosphorylation assays (TCR crosslinking), dominant-negative Itk expression, reporter assays, N-terminal deletion mapping European journal of immunology Medium 19701889
2011 OCA-B directly interacts with TFII-I (which binds DICE elements in Igh promoters); OCA-B relieves HDAC3-mediated Igh promoter repression by competing with HDAC3 for binding to promoter-bound TFII-I; Igh 3' enhancer-bound OCA-B and promoter-bound TFII-I mediate promoter–enhancer looping interactions in both cis and trans, required for Igh transcription. Co-immunoprecipitation, chromatin immunoprecipitation, chromosome conformation capture (looping assay), reporter assays, competition binding assays Molecular cell High 21549311
2014 Rev7 (regulatory subunit of Pol ζ) binds to TFII-I; TFII-I is required for translesion synthesis (TLS) and DNA damage tolerance independent of its transcription function; TLS function of TFII-I requires homodimerization and binding to PCNA, suggesting TFII-I bridges PCNA and Pol ζ. Co-immunoprecipitation, TLS functional assays, homodimerization mutants, PCNA-binding assays PLoS genetics Medium 24922507
2015 TFII-I interacts with CTCF in a distinct chromatin-bound complex; TFII-I is essential for directing CTCF binding to promoter-proximal regions of metabolic genes across the genome; knockdown of TFII-I reduces CTCF binding, diminishes CDK8 recruitment, and attenuates RNA Pol II Ser5 phosphorylation at co-regulated genes. Mass spectrometry of CTCF interactors, biochemical fractionation, ChIP-seq, siRNA knockdown, Pol II phosphorylation assay Proceedings of the National Academy of Sciences of the United States of America High 25646466
2015 TFII-I is SUMOylated at K221 and K240 by SUMO1; PIAS4 acts as the E3 ligase for TFII-I SUMOylation; SENP2 deSUMOylates TFII-I; SUMOylation reduces TFII-I binding to HDAC3, thereby promoting TFII-I transcriptional activity; SUMOylation is critical for TFII-I-driven cell proliferation and colony formation. Large-scale proteomics/IP-Western blot validation, site-directed mutagenesis (K221R, K240R), immunoprecipitation, cell proliferation assays, colony formation assays Journal of proteome research Medium 25869096
2016 Adenovirus E4-ORF3 stimulates SUMOylation of TFII-I early during infection, then triggers its ubiquitination and proteasomal degradation; E4-ORF3 is required for TFII-I ubiquitination; degradation of TFII-I by E4-ORF3 stimulates activity of a TFII-I-repressed viral promoter. Co-immunoprecipitation, ubiquitination assays, proteasome inhibitor experiments, reporter assays, infection experiments mBio Medium 26814176
2019 Selective deletion of Gtf2i in excitatory neurons of the mouse forebrain causes reduced mature oligodendrocyte numbers, reduced myelin thickness, and impaired axonal conductivity; ~70% of genes with decreased mRNA in mutant cortex are myelination-related; restoring myelination with clemastine or increasing axonal conductivity rescued the behavioral deficits (increased sociability, fine motor deficits, anxiety). Conditional neuron-specific knockout, mRNA-seq, electron microscopy of myelin, electrophysiology, pharmacological rescue with clemastine Nature neuroscience High 31011227
2023 GTF2I dosage controls dynamics of neural progenitor proliferation and excitatory neuron differentiation in cortical organoids; 7q11.23 duplication (extra GTF2I copy) causes precocious excitatory neuron production rescued by restoring physiological GTF2I levels; GTF2I acts through LSD1 (lysine demethylase 1) as a downstream effector, and LSD1 inhibition rescues ASD-like behaviors in transgenic Gtf2i-duplication mice. Patient-derived cortical organoids, single-cell RNA-seq, proteomics, transgenic mouse model, LSD1 inhibitor treatment, behavioral assays Science advances High 38019906
2020 The GTF2I L424H knock-in mutation in thymic epithelial cells causes cell transformation, aneuploidy, and increased tumor growth; mutant TFII-I upregulates glycolytic enzymes and cyclooxygenase-2 (COX-2), and COX-2 upregulation is required for cell survival under metabolic stress and for cellular transformation. Gtf2i L424H knock-in cells, transcriptome analysis, cell transformation assays, COX-2 functional inhibition, metabolic stress assays Cell death and differentiation Medium 32034314
2022 Conditional knock-in of Gtf2i L424H in Foxn1+ thymic epithelial cells impairs thymic medulla development and maturation of medullary thymic epithelial cells (mTECs), causes enrichment of E2F/MYC target gene signatures, and leads to thymoma formation in aged mice, establishing the mutation as a driver of thymic epithelial transformation. Conditional knock-in mouse model, digital spatial transcriptomic profiling (GeoMx), immunohistochemistry, TCR repertoire analysis Journal of thoracic oncology Medium 36049655
2008 TFII-I interacts with Elongin A (identified by pull-down assay); TFII-I binds upstream and downstream of transcription start sites at active and repressed genes respectively; at the ATF3 stress-responsive gene, TFII-I is required for induction of transcription and correlates with increased Pol II and Elongin A association, implicating TFII-I in transcription elongation. Biotinylation-tagging ChIP-seq, pull-down assays, siRNA knockdown, Pol II/Elongin A ChIP Nucleic acids research Medium 24875474

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1993 Direct role for Myc in transcription initiation mediated by interactions with TFII-I. Nature 252 8377829
2014 A specific missense mutation in GTF2I occurs at high frequency in thymic epithelial tumors. Nature genetics 218 24974848
1997 Cloning of an inr- and E-box-binding protein, TFII-I, that interacts physically and functionally with USF1. The EMBO journal 175 9384587
1993 An alternative pathway for transcription initiation involving TFII-I. Nature 153 8377828
1997 BAP-135, a target for Bruton's tyrosine kinase in response to B cell receptor engagement. Proceedings of the National Academy of Sciences of the United States of America 149 9012831
1998 A duplicated gene in the breakpoint regions of the 7q11.23 Williams-Beuren syndrome deletion encodes the initiator binding protein TFII-I and BAP-135, a phosphorylation target of BTK. Human molecular genetics 139 9466987
2003 GTF2I hemizygosity implicated in mental retardation in Williams syndrome: genotype-phenotype analysis of five families with deletions in the Williams syndrome region. American journal of medical genetics. Part A 128 14556246
1997 A multifunctional DNA-binding protein that promotes the formation of serum response factor/homeodomain complexes: identity to TFII-I. Genes & development 119 9334314
1998 TFII-I enhances activation of the c-fos promoter through interactions with upstream elements. Molecular and cellular biology 101 9584171
2008 Essential functions of the Williams-Beuren syndrome-associated TFII-I genes in embryonic development. Proceedings of the National Academy of Sciences of the United States of America 99 19109438
2019 Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drug. Nature neuroscience 97 31011227
2009 Partial 7q11.23 deletions further implicate GTF2I and GTF2IRD1 as the main genes responsible for the Williams-Beuren syndrome neurocognitive profile. Journal of medical genetics 97 19897463
2001 Biochemistry and biology of the inducible multifunctional transcription factor TFII-I. Gene 97 11674993
2003 Williams syndrome deficits in visual spatial processing linked to GTF2IRD1 and GTF2I on chromosome 7q11.23. Genetics in medicine : official journal of the American College of Medical Genetics 94 12865760
2001 Identification of TFII-I as the endoplasmic reticulum stress response element binding factor ERSF: its autoregulation by stress and interaction with ATF6. Molecular and cellular biology 92 11287625
1999 Regulation of nuclear localization and transcriptional activity of TFII-I by Bruton's tyrosine kinase. Molecular and cellular biology 91 10373551
2009 Is it Williams syndrome? GTF2IRD1 implicated in visual-spatial construction and GTF2I in sociability revealed by high resolution arrays. American journal of medical genetics. Part A 88 19205026
2010 Haploinsufficiency of Gtf2i, a gene deleted in Williams Syndrome, leads to increases in social interactions. Autism research : official journal of the International Society for Autism Research 85 21328569
2006 Action of TFII-I outside the nucleus as an inhibitor of agonist-induced calcium entry. Science (New York, N.Y.) 80 17023658
2002 Physical and functional interactions of histone deacetylase 3 with TFII-I family proteins and PIASxbeta. Proceedings of the National Academy of Sciences of the United States of America 79 12239342
2005 Transcriptional regulation of the Grp78 promoter by endoplasmic reticulum stress: role of TFII-I and its tyrosine phosphorylation. The Journal of biological chemistry 65 15664986
2000 Isolation and characterization of BEN, a member of the TFII-I family of DNA-binding proteins containing distinct helix-loop-helix domains. Proceedings of the National Academy of Sciences of the United States of America 62 10861001
2015 Genome-wide targeting of the epigenetic regulatory protein CTCF to gene promoters by the transcription factor TFII-I. Proceedings of the National Academy of Sciences of the United States of America 60 25646466
2012 Duplication of GTF2I results in separation anxiety in mice and humans. American journal of human genetics 59 22578324
2008 The complex of TFII-I, PARP1, and SFPQ proteins regulates the DYX1C1 gene implicated in neuronal migration and dyslexia. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 59 18445785
2002 cGMP-dependent protein kinase I beta physically and functionally interacts with the transcriptional regulator TFII-I. The Journal of biological chemistry 56 12082086
2002 Histone deacetylase 3 binds to and regulates the multifunctional transcription factor TFII-I. The Journal of biological chemistry 56 12393887
1998 TFII-I regulates Vbeta promoter activity through an initiator element. Molecular and cellular biology 56 9671454
2000 Extracellular signal-regulated kinase binds to TFII-I and regulates its activation of the c-fos promoter. Molecular and cellular biology 53 10648599
2011 Direct interactions of OCA-B and TFII-I regulate immunoglobulin heavy-chain gene transcription by facilitating enhancer-promoter communication. Molecular cell 52 21549311
2006 Induction of immunoglobulin heavy-chain transcription through the transcription factor Bright requires TFII-I. Molecular and cellular biology 52 16738337
2012 Association of GTF2i in the Williams-Beuren syndrome critical region with autism spectrum disorders. Journal of autism and developmental disorders 51 22048961
2002 c-Src-dependent transcriptional activation of TFII-I. The Journal of biological chemistry 50 11934902
2000 Alternatively spliced isoforms of TFII-I. Complex formation, nuclear translocation, and differential gene regulation. The Journal of biological chemistry 50 10854432
2007 Signal-induced functions of the transcription factor TFII-I. Biochimica et biophysica acta 48 17976384
2007 Induction of chromosomally integrated HIV-1 LTR requires RBF-2 (USF/TFII-I) and Ras/MAPK signaling. Virus genes 47 17546494
2005 TFII-I regulates induction of chromosomally integrated human immunodeficiency virus type 1 long terminal repeat in cooperation with USF. Journal of virology 45 15767439
2004 Isolation and characterisation of GTF2IRD2, a novel fusion gene and member of the TFII-I family of transcription factors, deleted in Williams-Beuren syndrome. European journal of human genetics : EJHG 45 15100712
2017 Pathophysiology of TFII-I: Old Guard Wearing New Hats. Trends in molecular medicine 44 28461154
1998 Regulation of TFII-I activity by phosphorylation. The Journal of biological chemistry 43 9837922
1996 NF-kappa B homodimer binding within the HIV-1 initiator region and interactions with TFII-I. Proceedings of the National Academy of Sciences of the United States of America 42 8901589
2008 Identification of the TFII-I family target genes in the vertebrate genome. Proceedings of the National Academy of Sciences of the United States of America 40 18579769
2005 Phosphoproteome profiling of transforming growth factor (TGF)-beta signaling: abrogation of TGFbeta1-dependent phosphorylation of transcription factor-II-I (TFII-I) enhances cooperation of TFII-I and Smad3 in transcription. Molecular biology of the cell 38 16055503
2005 Positive and negative regulation of the transforming growth factor beta/activin target gene goosecoid by the TFII-I family of transcription factors. Molecular and cellular biology 38 16055724
2004 Comparison of TFII-I gene family members deleted in Williams-Beuren syndrome. Protein science : a publication of the Protein Society 38 15388857
2014 The transcription factor TFII-I promotes DNA translesion synthesis and genomic stability. PLoS genetics 37 24922507
2003 Regulation of immunoglobulin promoter activity by TFII-I class transcription factors. The Journal of biological chemistry 36 14645227
1998 A mouse single-copy gene, Gtf2i, the homolog of human GTF2I, that is duplicated in the Williams-Beuren syndrome deletion region. Genomics 35 9521869
1995 The TATA-less promoter of mouse ribonucleotide reductase R1 gene contains a TFII-I binding initiator element essential for cell cycle-regulated transcription. The Journal of biological chemistry 35 8530424
2005 Inhibition of TFII-I-dependent cell cycle regulation by p53. Molecular and cellular biology 34 16314517
2000 Characterization and gene structure of a novel retinoblastoma-protein-associated protein similar to the transcription regulator TFII-I. The Biochemical journal 34 10642537
2017 A new GTF2I-BRAF fusion mediating MAPK pathway activation in pilocytic astrocytoma. PloS one 33 28448514
2014 17β-Estradiol inhibits ER stress-induced apoptosis through promotion of TFII-I-dependent Grp78 induction in osteoblasts. Laboratory investigation; a journal of technical methods and pathology 33 24933421
2000 Structure-function analysis of TFII-I. Roles of the N-terminal end, basic region, and I-repeats. The Journal of biological chemistry 33 11113127
2015 Intracisternal Gtf2i Gene Therapy Ameliorates Deficits in Cognition and Synaptic Plasticity of a Mouse Model of Williams-Beuren Syndrome. Molecular therapy : the journal of the American Society of Gene Therapy 32 26216516
2004 TFII-I, a candidate gene for Williams syndrome cognitive profile: parallels between regional expression in mouse brain and human phenotype. Neuroscience 32 14751286
2014 Cognitive-behavioral phenotypes of Williams syndrome are associated with genetic variation in the GTF2I gene, in a healthy population. BMC neuroscience 31 25429715
2009 Transcription factor TFII-I causes transcriptional upregulation of GRP78 synthesis in prostate cancer cells. Journal of cellular biochemistry 31 19097122
2005 Vascular endothelial growth factor receptor-2: counter-regulation by the transcription factors, TFII-I and TFII-IRD1. The Journal of biological chemistry 31 15941713
2023 GTF2I dosage regulates neuronal differentiation and social behavior in 7q11.23 neurodevelopmental disorders. Science advances 30 38019906
2020 Mutant GTF2I induces cell transformation and metabolic alterations in thymic epithelial cells. Cell death and differentiation 30 32034314
1999 The human KDR/flk-1 gene contains a functional initiator element that is bound and transactivated by TFII-I. The Journal of biological chemistry 30 9915861
2010 Essential role of the N-terminal region of TFII-I in viability and behavior. BMC medical genetics 29 20403157
2005 TFII-I and USF (RBF-2) regulate Ras/MAPK-responsive HIV-1 transcription in T cells. European journal of cancer (Oxford, England : 1990) 29 16223582
2002 Genomic organization of the genes Gtf2ird1, Gtf2i, and Ncf1 at the mouse chromosome 5 region syntenic to the human chromosome 7q11.23 Williams syndrome critical region. Genomics 29 11827466
2005 Identification of the interface between cGMP-dependent protein kinase Ibeta and its interaction partners TFII-I and IRAG reveals a common interaction motif. The Journal of biological chemistry 28 16166082
2002 The SUMO ubiquitin-protein isopeptide ligase family member Miz1/PIASxbeta /Siz2 is a transcriptional cofactor for TFII-I. The Journal of biological chemistry 28 12193603
2001 JAK2 activates TFII-I and regulates its interaction with extracellular signal-regulated kinase. Molecular and cellular biology 28 11313464
2001 Repression of TFII-I-dependent transcription by nuclear exclusion. Proceedings of the National Academy of Sciences of the United States of America 26 11438732
2015 Variation in the Williams syndrome GTF2I gene and anxiety proneness interactively affect prefrontal cortical response to aversive stimuli. Translational psychiatry 25 26285132
2010 Molecular basis of Williams-Beuren syndrome: TFII-I regulated targets involved in craniofacial development. The Cleft palate-craniofacial journal : official publication of the American Cleft Palate-Craniofacial Association 25 20500075
2005 Multiple GTF2I-like repeats of general transcription factor 3 exhibit DNA binding properties. Evidence for a common origin as a sequence-specific DNA interaction module. The Journal of biological chemistry 25 15987678
2020 Functions of Gtf2i and Gtf2ird1 in the developing brain: transcription, DNA binding and long-term behavioral consequences. Human molecular genetics 24 32313931
2011 Multifunctional transcription factor TFII-I is an activator of BRCA1 function. British journal of cancer 24 21407215
2009 Characterization of a novel interaction between transcription factor TFII-I and the inducible tyrosine kinase in T cells. European journal of immunology 24 19701889
2008 Specific interaction of TFII-I with an upstream element on the HIV-1 LTR regulates induction of latent provirus. FEBS letters 24 18976654
2003 Expression of BEN, a member of TFII-I family of transcription factors, during mouse pre- and postimplantation development. Gene expression patterns : GEP 24 12971990
2020 Primary Driver Mutations in GTF2I Specific to the Development of Thymomas. Cancers 23 32722121
2004 GTF2IRD2 is located in the Williams-Beuren syndrome critical region 7q11.23 and encodes a protein with two TFII-I-like helix-loop-helix repeats. Proceedings of the National Academy of Sciences of the United States of America 23 15243160
2017 The Williams syndrome prosociality gene GTF2I mediates oxytocin reactivity and social anxiety in a healthy population. Biology letters 22 28424317
2016 The Adenovirus E4-ORF3 Protein Stimulates SUMOylation of General Transcription Factor TFII-I to Direct Proteasomal Degradation. mBio 22 26814176
2015 Functional Proteomics Study Reveals SUMOylation of TFII-I is Involved in Liver Cancer Cell Proliferation. Journal of proteome research 22 25869096
2001 Identification of phosphorylation sites for Bruton's tyrosine kinase within the transcriptional regulator BAP/TFII-I. The Journal of biological chemistry 22 11373296
2019 Gtf2i and Gtf2ird1 mutation do not account for the full phenotypic effect of the Williams syndrome critical region in mouse models. Human molecular genetics 21 31418010
2012 Diversity and complexity in chromatin recognition by TFII-I transcription factors in pluripotent embryonic stem cells and embryonic tissues. PloS one 21 22970219
2007 Recruitment of coregulator complexes to the beta-globin gene locus by TFII-I and upstream stimulatory factor. The FEBS journal 21 17970752
2003 Mechanism of Bruton's tyrosine kinase-mediated recruitment and regulation of TFII-I. The Journal of biological chemistry 21 14623887
2009 Phase specific functions of the transcription factor TFII-I during cell cycle. Cell cycle (Georgetown, Tex.) 20 19182516
2007 TFII-I gene family during tooth development: candidate genes for tooth anomalies in Williams syndrome. Developmental dynamics : an official publication of the American Association of Anatomists 20 17823943
2004 The early embryonic expression of TFII-I during mouse preimplantation development. Gene expression patterns : GEP 20 14678824
2022 A Knock-In Mouse Model of Thymoma With the GTF2I L424H Mutation. Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer 19 36049655
2020 High-throughput screening identifies histone deacetylase inhibitors that modulate GTF2I expression in 7q11.23 microduplication autism spectrum disorder patient-derived cortical neurons. Molecular autism 19 33208191
2014 Genomic and proteomic analysis of transcription factor TFII-I reveals insight into the response to cellular stress. Nucleic acids research 19 24875474
2022 Human thymoma-associated mutation of the GTF2I transcription factor impairs thymic epithelial progenitor differentiation in mice. Communications biology 18 36175547
2018 The contribution of GTF2I haploinsufficiency to Williams syndrome. Molecular and cellular probes 18 29305905
2006 TFII-I down-regulates a subset of estrogen-responsive genes through its interaction with an initiator element and estrogen receptor alpha. Genes to cells : devoted to molecular & cellular mechanisms 18 16611241
1997 Methods for studying the biochemical properties of an Inr element binding protein: TFII-I. Methods (San Diego, Calif.) 18 9237169
2013 TFII-I regulates target genes in the PI-3K and TGF-β signaling pathways through a novel DNA binding motif. Gene 17 23831514
2009 Williams-Beuren syndrome-associated transcription factor TFII-I regulates osteogenic marker genes. The Journal of biological chemistry 17 19880526
2007 Cutting Edge: TFII-I controls B cell proliferation via regulating NF-kappaB. Journal of immunology (Baltimore, Md. : 1950) 17 17312101

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