| 1997 |
The N-terminal domain of yeast TAF4 (yTAF(II)130) binds TBP with high affinity (Kd ~1 nM), and this interaction is physiologically significant for cell growth; furthermore, the N-terminal domain actively dissociates TBP from TATA box-containing DNA. |
Coimmunoprecipitation, protein blotting, fluorescence anisotropy spectroscopy, genetic complementation of taf130Δ null allele |
Molecular and cellular biology |
High |
9154807
|
| 1997 |
Human TAF(II)135 potentiates transcriptional activation by the AF-2 of retinoic acid, thyroid hormone, and vitamin D3 receptors (RAR, TR, VDR) but not by estrogen or RXR receptors; the coactivator activity maps to a region between two conserved domains. |
Mammalian cell overexpression transcriptional assays with receptor-specific reporters |
Genes & development |
Medium |
9192867
|
| 1997 |
The C-terminal 105 amino acids of hTAF(II)135 directly bind the CR3 activation domain of adenovirus E1A, and overexpression of this C-terminal fragment blocks E1A-inducible transcriptional activation in vivo. |
In vitro protein-protein interaction (pulldown), in vivo transcriptional reporter assay |
Journal of virology |
Medium |
9311891
|
| 1997 |
The proline-rich N-terminal activation domain of p45NF-E2 binds specifically to TAFII130, and this interaction is required for enhancer-dependent transcription of the alpha- and beta-globin loci. |
Protein-protein interaction studies, mutational analysis, transient transcription assays in NF-E2 null cell line, endogenous locus reactivation |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
9294161
|
| 1998 |
Distinct subdomains of hTAFII130 mediate interactions with different activation domains: the Q1 region interacts with Sp1B; Q1-Q4 interact with Sp1A; Q1-Q2 interact with the N-terminal activation domain of CREB. Overexpression of the Q1-Q4 region in HeLa cells inhibits Sp1- but not VP16-mediated transcription. |
Yeast two-hybrid, deletion mutagenesis, in vivo transcriptional repression assay in HeLa cells |
Molecular and cellular biology |
High |
9742090
|
| 2000 |
Expanded polyglutamine stretches preferentially bind TAFII130 and suppress CREB-dependent transcription; co-expression of TAFII130 restores CREB-dependent transcription and rescues polyQ-induced cell death. |
Protein-protein interaction assays, transcriptional reporter assays, cell viability assays with polyQ constructs |
Nature genetics |
High |
10973244
|
| 2001 |
hTAFII130 serves as a coactivator for NFATp: it binds directly to the C-terminal domain (aa 688–921) of NFATp, and a partial TFIID complex (TBP + TAF250 + TAF130) supports NFATp-activated transcription in vitro. |
Reconstituted in vitro transcription assay, in vitro pulldown interaction assay, overexpression in Cos-1 cells |
Molecular and cellular biology |
High |
11313476
|
| 2001 |
TBP and TAFII135 are selectively depleted during retinoic acid-induced differentiation of F9 embryonal carcinoma cells via targeted proteasome-mediated proteolysis; ectopic TAFII135 expression delays RARγ2 proteolysis and impairs differentiation. |
Western blotting, proteasome inhibitor treatment, gain-of-function overexpression, differentiation marker assays |
BMC molecular biology |
Medium |
11285139
|
| 2002 |
hTAFII130 interacts with HP1alpha and HP1gamma (but not HP1beta) in an isoform-specific manner through a pentapeptide HP1-binding motif; mutation of this motif abolishes the interaction. Gal4-HP1 proteins interfere with hTAFII130-mediated transcriptional activation. |
Yeast two-hybrid, GST pulldown of endogenous TFIID components from HeLa nuclear extracts, HP1-binding motif mutagenesis, transcriptional reporter assay |
Proceedings of the National Academy of Sciences of the United States of America |
High |
11959914
|
| 2002 |
The histone-fold domain (HFD) and a short conserved C-terminal domain (CCTD) of yTAF4 are both required for heterodimerization with yTAF12; temperature-sensitive mutations in the HFD α2 helix or CCTD are suppressed by overexpression of yTAF12. Crystal structure of the hTAF4-hTAF12 histone-like heterodimer reveals an atypical HFD organization where the α3 helix lies within the CCTD. |
Genetic complementation (ts alleles + overexpression suppression), coexpression in E. coli to test direct heterodimerization, X-ray crystallography |
The Journal of biological chemistry |
High |
12237303
|
| 2002 |
Mutant huntingtin interacts with transcriptional activator Sp1 and coactivator TAFII130; co-expression of Sp1 and TAFII130 reverses huntingtin-induced transcriptional inhibition of the dopamine D2 receptor gene and protects neurons from huntingtin-induced toxicity. |
Co-immunoprecipitation, transcriptional reporter assay in striatal cell cultures, neuroprotection assay, DNA-binding assay in postmortem HD brain |
Science |
High |
11988536
|
| 2005 |
TAF4 inactivation in mouse embryonic fibroblasts deregulates >1000 genes, activates TGF-β signalling and autocrine growth; TAF4 is an essential cofactor for activation by RAR and CREB but not for Sp1 or the vitamin D3 receptor. Loss of TAF4 is compensated by TAF4b-containing TFIID. |
Conditional gene inactivation (Taf4−/− MEFs), microarray expression profiling, transcriptional assays |
The EMBO journal |
High |
16015375
|
| 2005 |
RanBPM is a co-factor of TAF4 in neural progenitor cells; endogenous TAF4 and RanBPM co-immunoprecipitate from neural stem cell extracts. Co-transfection of TAF4 and RanBPM increases primary neurite processes, an effect lost with a TAF4 isoform lacking the RanBPM-interacting domain. |
Yeast two-hybrid/protein interaction screen, co-immunoprecipitation, co-transfection morphological assay |
Molecular and cellular neurosciences |
Medium |
15911349
|
| 2006 |
TAF4 is the most critical subunit for maintaining the stability of the TFIID complex in Drosophila; RNAi knockdown of TAF4 destabilizes holo-TFIID more than knockdown of TBP or TAF1. TAF4 and TAF1 specifically mediate transcription from TATA-less, DPE-containing promoters, whereas TATA-containing promoters are less dependent on these subunits. |
RNAi knockdown of individual TFIID subunits in Drosophila S2 cells, in vitro transcription assays with TATA-less vs. TATA-containing promoter reporters |
Proceedings of the National Academy of Sciences of the United States of America |
High |
16895980
|
| 2007 |
The TAF-homology (TAFH) domain of ETO, related in sequence to TAF4, has a structure similar to yeast Rpb4 and E. coli σ70 and acts as a docking platform: overlapping surfaces interact with a repression domain of N-CoR and with an activation domain from E-box transcription factors, enabling interchange of positive and negative coregulators. |
X-ray crystallography of ETO-TAFH domain, protein-protein interaction mapping |
Nature structural & molecular biology |
Medium |
17572682
|
| 2007 |
TAF4 inactivation in basal keratinocytes reduces expression of skin barrier genes, causes hair cycle defects, and promotes malignant transformation; TAF4 has cell-autonomous and non-cell-autonomous tumour suppressor activity in mouse epidermis. |
Conditional Cre-lox Taf4 inactivation in keratinocytes, gene expression analysis, chemical carcinogenesis assay |
Development (Cambridge, England) |
Medium |
17626060
|
| 2008 |
OMA-1 and OMA-2 in C. elegans repress transcription in germline blastomeres P0 and P1 by binding to and sequestering TAF-4 in the cytoplasm, preventing its incorporation into TFIID and the pol II preinitiation complex. This binding requires phosphorylation of OMA-1/2 by the DYRK kinase MBK-2, activated at meiosis II after fertilization. |
Genetic epistasis, biochemical binding assays, live imaging, ectopic expression experiments in C. elegans embryos |
Cell |
High |
18854162
|
| 2008 |
The ETO coactivation domain of TAF4 is targeted by Wnt/Wingless signalling through Pygopus in Drosophila; expression of TAF4 lacking the ETO domain specifically impairs Wingless-induced transcription of naked cuticle. |
Generation of altered holo-TFIID in Drosophila by ETO-domain deletion, in vivo transcription assay |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
19116271
|
| 2009 |
The TAF4/4b–TAF12 complex binds DNA with high affinity requiring ~70 bp length but with only weak sequence preference; a DNA-binding mutant of TAF4 reduces TFIID occupancy and Initiator activity at a subset of TATA-box/Initiator-containing promoters. |
In vitro DNA-binding assays, expression profiling of wild-type vs. DNA-binding mutant TAF4 cells, ChIP for TFIID occupancy |
The Journal of biological chemistry |
High |
19635797
|
| 2013 |
TAF4 directly interacts with the E-protein activation domain 3 (AD3) through its TAFH domain; this interaction enhances TFIID binding to core promoters and is required for activation of natural E-protein target genes. The TAFH domain has a gene-specific role in TFIID recruitment in vivo. |
Biochemical pulldown assays, ChIP, gene expression analysis, domain-specific mutagenesis |
Genes & development |
High |
23873942
|
| 2013 |
TAF4b (but not TAF4) interacts with the pluripotency factor Oct4 in embryonic stem cells; TAF4b cooperates with Oct4 to regulate a subset of genes (including Sohlh2 and Yes1), whereas TAF4 inhibits ESC proliferation and is required for later differentiation stages. |
Co-immunoprecipitation, knockdown (siRNA), expression profiling |
Genes to cells |
Medium |
23350932
|
| 2014 |
The TAF4–TAF12 heterodimer interacts directly with HNF4A, and TAF4 is required in vivo to maintain HNF4A-directed gene expression and to promote HNF4A occupancy at cis-regulatory elements near transcription start sites of post-natal liver function genes; TAF4 promotes preinitiation complex formation at these promoters. |
Liver-specific Taf4 inactivation in mice, ChIP-seq, RNA-seq, direct protein interaction assay |
eLife |
High |
25209997
|
| 2016 |
Taf4a−/− embryos survive until E9.5 with primary germ layers intact, but require TAF4 for trunk/anterior patterning and ventral morphogenesis. Taf4a−/− embryonic stem cells contain TAF4b-containing TFIID but fail to complete differentiation into glutamatergic neurons and cardiomyocytes due to impaired preinitiation complex formation at critical differentiation gene promoters. |
Taf4a gene inactivation in mice, embryo analysis, ESC in vitro differentiation assays, ChIP for PIC formation |
Nature communications |
High |
27026076
|
| 2016 |
Interaction between the Q1 glutamine-rich region of TAF4 and the Q-rich region of Sp1 occurs through intrinsically disordered regions without significant coupled folding; binding sites are localized to defined 20-30 residue stretches identified by NMR chemical shift perturbation. |
NMR spectroscopy (heteronuclear, 13C chemical shift analysis), surface plasmon resonance |
Protein science |
Medium |
27515574 28857320
|
| 2021 |
TAF4 inactivation in adult pancreatic beta cells impairs critical beta-cell function genes, decreases insulin secretion, and causes trans-differentiation of beta cells into alpha-like cells as revealed by single-cell RNA-seq; computational analysis implicates the NuRF chromatin remodelling complex alongside critical beta-cell transcription factors in this process. |
Beta-cell specific Taf4 inactivation in mice, single-cell RNA-seq, glucose tolerance tests, plasma insulin measurement |
Cell death & disease |
Medium |
34385420
|
| 2023 |
TAF4 inactivation in intestinal epithelium increases PRC2 (Ezh2/Suz12) activity in enteroid stem/progenitor cells; pharmacological inhibition of Ezh2 restores budding, cell proliferation, and the stem/progenitor compartment in Taf4-mutant enteroids, demonstrating that TAF4 antagonizes PRC2-mediated epigenetic silencing to maintain intestinal stem cell gene expression. |
Tissue-specific Taf4 inactivation, enteroid culture, ChIP for PRC2 components, Ezh2 inhibitor treatment, scRNA-seq |
Cell death and differentiation |
High |
36639541
|
| 2025 |
TAF4A forms a complex with the heterotrimeric transcription factor NF-Y in muscle stem cells and is required for cell-type-specific expression of Kansl2. TAF4A inactivation reduces Kansl2, alters lamin A/C post-translational modification (acetylation), decreases nuclear stiffness, disrupts nuclear architecture, and causes genomic instability, thereby depleting the stem cell pool and abolishing muscle regeneration. |
Muscle stem cell-specific Taf4a inactivation, co-immunoprecipitation, genome stability assays, nuclear mechanics measurements, gene expression analysis |
Nature communications |
High |
41028714
|