ArticleNature2013
The architecture of human general transcription factor TFIID core complex.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 160 citations in OpenAlex.
- Global transcriptional disturbances underlie Cornelia de Lange syndrome and related phenotypes.The Journal of clinical investigation · 2015Trial
- The molecular basis of transcription initiation by RNA polymerase II.Nature reviews. Molecular cell biology · 2026Review
- Dynamic partitioning of a critical elongation factor between LEC and SEC regulates cellular snRNA and proliferation-related mRNA transcription.Nature communications · 2026Article
- Evaluating the evolutionary relationship of TATA binding protein (TBP) with various folding patterns of protein domains using support vector machine (SVM).Scientific reports · 2026Article
- High-resolution binding data of TFIID and cofactors show promoter-specific differences in vivo.Research square · 2026Article
- Long non-coding RNA ZBTB46-AS1 promotes ovarian cancer progression through regulation of p53 activity by TAF6 protein.American journal of translational research · 2026Article
- High-resolution binding data of TFIID and cofactors show promoter-specific differencesbioRxiv : the preprint server for biology · 2025Article
- TheInternational journal of molecular sciences · 2025Review
- PROTAC-Mediated Degradation of TAF1 Induces Apoptosis in AML Cells and Inhibits Tumor Growth In Vivo.Molecular cancer therapeutics · 2025Article
- Article
- The phenotypic spectrum of the Cornelia de Lange-like "Alazami-Yuan syndrome": A case report of the 7th diagnosed individual and review of the literature.Clinical case reports · 2025Article
- RNA polymerase II transcription initiation in holo-TFIID-depleted mouse embryonic stem cells.Cell reports · 2024Article
- O-GlcNAc transferase congenital disorder of glycosylation (OGT-CDG): Potential mechanistic targets revealed by evaluating the OGT interactome.The Journal of biological chemistry · 2024Review
- Taenia solium TAF6 and TAF9 bind to a downstream promoter element present in the Tstbp1 gene core promoter.PloS one · 2024Article
- Article
- Hierarchical TAF1-dependent co-translational assembly of the basal transcription factor TFIID.Nature structural & molecular biology · 2023Article
- Deletion of taf1 and taf5 in zebrafish capitulate cardiac and craniofacial abnormalities associated with TAFopathies through perturbations in metabolism.Biology open · 2023Article
- Hierarchical TAF1-dependent co-translational assembly of the basal transcription factor TFIID.bioRxiv : the preprint server for biology · 2023Article
- De novo putative loss-of-function variants in TAF4 are associated with a neuro-developmental disorder.Human mutation · 2022Article
- Loss of TAF8 causes TFIID dysfunction and p53-mediated apoptotic neuronal cell death.Cell death and differentiation · 2022Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The initiation of gene transcription by RNA polymerase II is regulated by a plethora of proteins in human cells. The first general transcription factor to bind gene promoters is transcription factor IID (TFIID). TFIID triggers pre-initiation complex formation, functions as a coactivator by interacting with transcriptional activators and reads epigenetic marks. TFIID is a megadalton-sized multiprotein complex composed of TATA-box-binding protein (TBP) and 13 TBP-associated factors (TAFs). Despite its crucial role, the detailed architecture and assembly mechanism of TFIID remain elusive. Histone fold domains are prevalent in TAFs, and histone-like tetramer and octamer structures have been proposed in TFIID. A functional core-TFIID subcomplex was revealed in Drosophila nuclei, consisting of a subset of TAFs (TAF4, TAF5, TAF6, TAF9 and TAF12). These core subunits are thought to be present in two copies in holo-TFIID, in contrast to TBP and other TAFs that are present in a single copy, conveying a transition from symmetry to asymmetry in the TFIID assembly pathway. Here we present the structure of human core-TFIID determined by cryo-electron microscopy at 11.6 Å resolution. Our structure reveals a two-fold symmetric, interlaced architecture, with pronounced protrusions, that accommodates all conserved structural features of the TAFs including the histone folds. We further demonstrate that binding of one TAF8-TAF10 complex breaks the original symmetry of core-TFIID. We propose that the resulting asymmetric structure serves as a functional scaffold to nucleate holo-TFIID assembly, by accreting one copy each of the remaining TAFs and TBP.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.