Affinage

TAF9

Transcription initiation factor TFIID subunit 9 · UniProt Q16594

Length
264 aa
Mass
29.0 kDa
Annotated
2026-06-10
29 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TAF9 is a histone H3-like core subunit shared by the general transcription factor TFIID and the SAGA/STAGA histone acetyltransferase coactivator complex, where it acts as a structural scaffold and an activator-docking surface that couples gene-specific transcriptional signals to the RNA Pol II machinery (PMID:7667268, PMID:9726987, PMID:15899866). Within these complexes TAF9 heterodimerizes with TAF6 through histone-fold contacts reinforced by the C-terminal HEAT-repeat (TAF6C) interface, an interaction essential for assembly of the TAF5–TAF6–TAF9 module and for incorporation into stable TFIID (PMID:22696218); its conserved C-terminal region is dispensable for complex integrity in extracts but required for TFIID/SAGA promoter occupancy and preinitiation complex assembly genome-wide (PMID:24550006). TAF9 serves as a direct binding site for a recurrent acidic transactivation-domain motif found across multiple activators, including p53 (PMID:7761466), CIITA (PMID:9171108), GLI1/GLI2 (PMID:26282181), the viral activator VP16 (PMID:17035330), and Notch effectors via Su(H)/NICD (PMID:25015288), and conversely is targeted by the corepressor N-CoR, which blocks the TFIIB–TAF9 contact to prevent initiation (PMID:9611234). Beyond the basal machinery, TAF9 stabilizes p53 by competing with mdm2 for the p53 N-terminal activation domain, blocking p53 ubiquitination and driving p53-dependent growth arrest (PMID:11278372, PMID:12370832), and its acetylation state—set by deacetylation through HDAC1—governs promoter binding and transcriptional output at programs such as PU.1 and peroxisomal fatty acid β-oxidation genes (PMID:28572446, PMID:34925033). Although TAF9 depletion collapses other TAFs and disrupts TFIID integrity, it is not required for bulk mRNA synthesis, indicating gene-selective rather than global function (PMID:10866663, PMID:12837753).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1995 High

    Established TAF9 as a sequence-specific coactivator rather than a purely structural TAF by showing it directly receives the p53 activation signal and is a histone-H3-like component of TFIID.

    Evidence In vitro transcription with antibody inhibition and direct binding assays (p53 ADs); reciprocal Co-IP and domain mapping with TAFII80 plus H3 sequence analysis

    PMID:7667268 PMID:7761466

    Open questions at the time
    • Did not define the structural basis of the H3-like fold within TFIID
    • Did not establish which TFIID surface contacts the p53 AD
  2. 1997 Medium

    Generalized TAF9 as a shared activator-docking platform by showing CIITA uses its TAD to bind TAF9 with a functional consequence for MHC class II gene activation.

    Evidence Yeast two-hybrid, in vitro binding, site-directed mutagenesis, transcription assays

    PMID:9171108

    Open questions at the time
    • Single lab; did not map a shared binding motif across activators
    • Did not resolve whether CIITA acts through TFIID or SAGA-bound TAF9
  3. 1998 Medium

    Showed TAF9 is not confined to TFIID but is also a subunit of the STAGA/SAGA HAT coactivator, and that it can be a target for repression via N-CoR.

    Evidence Native complex isolation with HAT activity assay (STAGA); reciprocal in vivo/in vitro binding and functional transcription assay (N-CoR disrupting TFIIB–TAF9)

    PMID:9611234 PMID:9726987

    Open questions at the time
    • N-CoR interaction shown by a single lab
    • Did not determine how TAF9 partitions between TFIID and STAGA
  4. 2000 High

    Resolved whether TAF9 is globally essential for transcription, revealing it is dispensable for bulk mRNA synthesis even though its loss destabilizes other TAFs.

    Evidence Conditional (tet-repressible) gene targeting in DT40 cells with pulse-labeling, Northern and Western readouts

    PMID:10866663

    Open questions at the time
    • Did not identify which specific gene programs depend on TAF9
    • Possible compensation by TAF9L not assessed here
  5. 2001 High

    Defined a non-transcriptional role: TAF9 stabilizes p53 by competing with mdm2 for the p53 N-terminus, blocking ubiquitination and enforcing growth arrest.

    Evidence Co-IP, ubiquitination assay, growth assay, non-p53-binding mutant; UV-induced shift in p53–TAF9 vs p53–mdm2 association

    PMID:11278372

    Open questions at the time
    • Did not quantify the stoichiometry of the competition in vivo
    • Did not separate free TAF9 from TFIID-incorporated TAF9 in this function
  6. 2002 Medium

    Refined the p53/mdm2/TAF9 interplay, showing mdm2 occupancy gates p53 accessibility to TAF9 and that prior mdm2 binding can modulate subsequent TAF9 recruitment and p21 transactivation.

    Evidence Site-directed mutagenesis (Thr18–Asp21 bond), in vitro binding, cell-based p21 expression assays

    PMID:12370832

    Open questions at the time
    • Single lab; mechanism of mdm2-induced conformational modulation not structurally defined
  7. 2003 Medium

    Linked TAF9's histone-fold motif to TFIID structural integrity and uncovered partial redundancy with TAF9L, with TAF9L specialized toward repression.

    Evidence Conditional gene targeting, RNAi, Co-IP, expression analysis in DT40 cells

    PMID:12837753

    Open questions at the time
    • Degree of TAF9/TAF9L overlap at individual promoters not mapped
    • Single lab
  8. 2005 High

    Consolidated TAF9 as a dual TFIID/TFTC-SAGA subunit and showed TAF9 vs TAF9b differentially control apoptosis and distinct gene sets while both being essential.

    Evidence Mass spectrometry, Co-IP, siRNA, expression microarray, apoptosis assays

    PMID:15899866

    Open questions at the time
    • Mechanistic basis of differential p53 stabilization between paralogs not resolved
  9. 2005 Medium

    Placed TAF9 in a broader regulatory network through genetic interactions with Mediator, SWR-C chromatin remodeling, and elongation factors, implicating SAGA-context TAF9 in transcription elongation.

    Evidence Genome-wide synthetic genetic array with ts taf9 allele, ChIP, epistasis (yeast)

    PMID:16118188

    Open questions at the time
    • Genetic interactions do not establish direct physical mechanism
    • Elongation role inferred largely from RPS5
  10. 2006 Medium

    Demonstrated a conserved activator-binding motif on TAF9 by showing a viral protein (rv-cyclin) competitively displaces VP16 from TAF9 to inhibit activation.

    Evidence GST pulldown, in vitro interaction and transcription assays, point mutagenesis

    PMID:17035330

    Open questions at the time
    • Single lab; cellular relevance of competition not tested in host cells
  11. 2012 High

    Provided the structural basis for the TAF6–TAF9 interaction, showing the TAF6 C-terminal HEAT-repeat domain anchors TAF9 and is required for the TAF5–TAF6–TAF9 module and TFIID incorporation.

    Evidence 1.9 Å crystal structure of TAF6C with mutagenesis, Co-IP, and cellular stability assays

    PMID:22696218

    Open questions at the time
    • Did not capture TAF9 itself in the structure
    • Did not resolve how the module docks within intact TFIID
  12. 2014 Medium

    Separated complex assembly from promoter function by showing TAF9's conserved C-terminal region is dispensable for TAF9–TAF6 binding but essential for TFIID/SAGA promoter occupancy and preinitiation complex assembly; also extended TAF9 to Notch-dependent transcription.

    Evidence Transcriptome microarray, ChIP, epistasis (yeast Taf9 CRD); RNAi, epistasis, Co-IP and reporter assays for Drosophila E(y)1/TAF9 with NICD/Su(H)

    PMID:24550006 PMID:25015288

    Open questions at the time
    • Molecular role of the CRD at the promoter not defined
    • Whether Notch effectors use the same TAF9 motif as other activators not shown
  13. 2015 Medium

    Extended TAF9 activator docking to oncogenic GLI proteins and revealed competitive sequestration logic in which p53 outcompetes GLI1 for TAF9 to suppress GLI transactivation.

    Evidence Cell-free pulldown, Co-IP, gain/loss-of-binding mutagenesis, transformation and transactivation assays

    PMID:26282181

    Open questions at the time
    • Single lab; in vivo relevance of p53–GLI1 competition for TAF9 not established
  14. 2017 Medium

    Identified acetylation as a switch controlling TAF9 function: HDAC1-mediated deacetylation is required for promoter binding, TFIID integrity, and activation of specific programs such as PU.1.

    Evidence ChIP, HDAC inhibitor treatment, HDAC1 knockdown/overexpression, Co-IP, promoter-binding assays

    PMID:28572446

    Open questions at the time
    • Acetyltransferase writing TAF9 not identified
    • Acetylated lysine residues not mapped
  15. 2017 Medium

    Connected TAF9 to lipid metabolism by showing TRF2/TAF9 control peroxisomal fatty acid β-oxidation genes and lipid droplet properties, and added MAGEC2 as a candidate activator partner.

    Evidence RNAi/mutant analysis with RNA profiling and lipidomics (Drosophila fat body); Co-IP, GST pulldown, immunofluorescence (HCA587/MAGEC2–TAF9)

    PMID:28273089 PMID:29257297

    Open questions at the time
    • MAGEC2 interaction (Low confidence) lacks functional follow-up and reciprocal validation
    • Whether the metabolic program is TFIID- or SAGA-dependent not resolved
  16. 2021 Medium

    Demonstrated a physiological metabolic output of TAF9 acetylation control, showing HDAC1-driven TAF9 deacetylation promotes β-oxidation and protects against NAFLD.

    Evidence TAF9 gain/loss-of-function in vivo and in vitro, lipid droplet quantification, β-oxidation assays, pharmacological HDAC1 activation

    PMID:34925033

    Open questions at the time
    • Direct target genes mediating the metabolic effect not fully mapped
    • Single lab
  17. 2025 Medium

    Revealed regulation of TAF9 by a noncoding RNA and a pro-tumorigenic transcriptional output, with lncRNA938 controlling TAF9 nuclear localization and TAF9 activating TTK to drive EMT in hepatoblastoma.

    Evidence RIP, RNA pulldown, immunofluorescence, luciferase reporter, Western blot, in vitro/in vivo functional assays

    PMID:40841910

    Open questions at the time
    • Mechanism of lncRNA-controlled nuclear import not defined
    • Single lab; whether TTK activation is via TFIID or SAGA not addressed

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the acetylation/deacetylation cycle, partner competition, and complex partitioning are integrated to select specific gene programs in vivo remains unresolved.
  • The acetyltransferase that writes TAF9 acetylation and the modified residues are unidentified
  • No structure of TAF9 itself bound to an activator TAD
  • Rules governing TAF9 allocation between TFIID and SAGA at individual promoters unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 5 GO:0005198 structural molecule activity 3 GO:0098772 molecular function regulator activity 2 GO:0140223 general transcription initiation factor activity 2
Localization
GO:0005634 nucleus 2
Pathway
R-HSA-74160 Gene expression (Transcription) 4 R-HSA-4839726 Chromatin organization 2
Partners
CIITAGLI1HDAC1MDM2NCOR1P53TAF5TAF6
Complex memberships
STAGA/SAGA (TFTC)TFIID

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 TAFII31 (TAF9) directly binds the amino-terminal transcriptional activation domain of p53 and is required for p53-mediated transcriptional activation; antibodies against TAFII31 inhibit p53-activated but not basal transcription in vitro, establishing TAFII31 as a coactivator of p53. In vitro transcription assay, antibody inhibition, protein binding/interaction assays Proceedings of the National Academy of Sciences of the United States of America High 7761466
1995 TAFII31 (TAF9) is a component of TFIID and interacts with TAFII80 via TAFII80's N-terminal residues 1–100; TAF9 shows sequence similarity to histone H3, suggesting a histone-fold-based core structure within TFIID. Coimmunoprecipitation, domain-mapping mutagenesis, sequence analysis Proceedings of the National Academy of Sciences of the United States of America High 7667268
1998 TAFII31 (TAF9) is a component of the human STAGA complex (SPT3-TAFII31-GCN5-L), a histone acetyltransferase complex distinct from TFIID; STAGA is proposed as the human homologue of yeast SAGA. Co-immunoprecipitation, native complex isolation, histone acetyltransferase activity assay The Journal of biological chemistry High 9726987
1998 The corepressor N-CoR and its variants RIP13a and RIP13Δ1 directly interact with TAFII32 (TAF9) both in vivo and in vitro; this interaction involves N-CoR interaction domain II and results in a non-functional complex that ablates the TFIIB–TAFII32 interaction critical for transcription initiation. Co-immunoprecipitation, in vitro binding assay, site-directed mutagenesis, functional transcription assay Nucleic acids research Medium 9611234
1997 The transcriptional activation domain of CIITA interacts directly with TAFII32 (TAF9), and reduced CIITA binding to TAFII32 correlates with decreased transcriptional activation of MHC class II genes. Yeast two-hybrid, in vitro binding assay, site-directed mutagenesis, transcription assay Nucleic acids research Medium 9171108
2001 TAF(II)31 (TAF9) stabilizes p53 by competing with mdm2 for binding to p53's amino-terminal domain, thereby inhibiting mdm2-mediated ubiquitination of p53, increasing p53 levels, activating p53 transcriptional activity, and leading to p53-dependent growth arrest; UV-induced p53 stabilization coincides with increased p53–TAF(II)31 and decreased p53–mdm2 association. Co-immunoprecipitation, ubiquitination assay, cell growth assay, site-directed mutagenesis (non-p53-binding mutant) The Journal of biological chemistry High 11278372
2002 Mdm-2 blocks accessibility of p53 to TAF(II)31 (TAF9); disruption of the intramolecular Thr18–Asp21 hydrogen bond in p53 attenuates Mdm-2 binding without directly affecting TAF(II)31 binding, but prior Mdm-2 incubation modulates TAF(II)31 interaction with p53, facilitating TAF(II)31 recruitment and enhanced p21 transactivation. Site-directed mutagenesis, in vitro binding assay, cell-based transcription/p21 expression assay Oncogene Medium 12370832
2000 Depletion of cTAF(II)31 (TAF9) in chicken DT40 cells causes loss of most other TAFII subunits but does not significantly reduce total poly(A)+ mRNA transcription or prevent c-fos activation after serum starvation, indicating TAF9 is not essential for bulk mRNA transcription in metazoan cells. Conditional gene targeting (tetracycline-repressible), pulse-labeling transcription assay, Northern blot, Western blot Molecular and cellular biology High 10866663
2003 TAF9 depletion in DT40 cells severely disrupts TFIID integrity; the histone fold motif (HFM) of TAF9 is functionally important for TFIID assembly; TAF9 and TAF9L are partly redundant, but TAF9L plays a role in transcriptional repression/silencing. Conditional gene targeting, RNA interference, co-immunoprecipitation, gene expression analysis The Journal of biological chemistry Medium 12837753
2005 TAF9 is a shared subunit of both TFIID and TFTC/SAGA complexes; TAF9b (TAF9L) is a paralog that also integrates into these complexes; TAF9 and TAF9b have differential roles in apoptosis regulation (differential p53 stabilization) and regulate distinct but partially overlapping gene sets; both are essential for cell viability. Mass spectrometry, Co-IP, siRNA knockdown, gene expression microarray, apoptosis assay Molecular and cellular biology High 15899866
2005 TAF9 genetically interacts with Mediator, chromatin modification/remodeling complexes (including all nonessential SWR-C subunits), regulators of transcription elongation, and G1/S cell cycle genes; TAF9 and SWR-C are both required for expression of the housekeeping gene RPS5, suggesting a role in transcription elongation in the context of SAGA. Genome-wide synthetic genetic array (SGA) using temperature-sensitive taf9 allele, chromatin immunoprecipitation, epistasis analysis Genetics Medium 16118188
2006 Walleye dermal sarcoma virus retroviral cyclin (rv-cyclin) directly binds TAF9 via a conserved motif present in multiple TAF9-binding transcriptional activators, competitively interfering with VP16–TAF9 interaction and inhibiting VP16-dependent transcription. GST pulldown, in vitro protein–protein interaction assay, transcription assay, point mutagenesis Journal of virology Medium 17035330
2012 The conserved C-terminal HEAT repeat domain (TAF6C) of TAF6 is required for the TAF6–TAF9 interaction within TFIID; HEAT repeat mutations in TAF6C disrupt TAF6–TAF9 binding and more strongly disrupt formation of the TAF5–TAF6–TAF9 trimeric complex; these mutations cause instability of TAF6 in cells, indicating poor TFIID incorporation. Crystal structure of TAF6C at 1.9 Å, site-directed mutagenesis, Co-IP, cell-based stability assay The Journal of biological chemistry High 22696218
2014 The conserved C-terminal region domain (CRD) of TAF9 (yeast Taf9) is required for TFIID and SAGA occupancy at promoters and for transcriptional activation genome-wide; the CRD is not needed for Taf9–Taf6 interaction or complex integrity in extracts, but is essential for preinitiation complex assembly at promoters. Transcriptome microarray, chromatin immunoprecipitation (ChIP), genetic epistasis with spt20Δ Molecular and cellular biology Medium 24550006
2014 Drosophila E(y)1/TAF9 interacts with the Notch intracellular domain (NICD) and Suppressor of Hairless [Su(H)] to facilitate transcriptional output of Notch signaling; genetic epistasis places E(y)1/TAF9 downstream of Notch cleavage; E(y)1/TAF9 knockdown causes Notch-mutant-like phenotypes in follicle cells and wing discs. In vivo RNAi screen, epistasis analysis, co-immunoprecipitation in S2 cells, reporter gene assay Journal of cell science Medium 25015288
2015 TAF9 directly binds GLI1 and GLI2 (but not GLI3) oncoproteins via their acidic α-helical transactivation domains; GLI1–TAF9 binding is required for oncogenic cell transformation; p53 binds TAF9 with higher affinity than GLI1 and sequesters TAF9 from GLI1, thereby inhibiting GLI-induced transactivation. Cell-free pulldown assay, co-immunoprecipitation, site-directed mutagenesis (point mutations abolishing or establishing TAF9 binding), cell transformation assay, transactivation assay DNA repair Medium 26282181
2017 HDAC1 deacetylates TAF9; acetylated TAF9 fails to bind to promoters and causes disassociation of the TFIID complex and transcriptional repression; deacetylation of TAF9 by HDAC1 is required for TFIID recruitment and activation of PU.1 transcription. ChIP, HDAC inhibitor treatment (acetylation increase), HDAC1 knockdown/overexpression, co-immunoprecipitation, promoter-binding assay FASEB journal Medium 28572446
2017 Drosophila TRF2 and TAF9 cooperatively regulate lipid droplet size and phospholipid fatty acid composition in the larval fat body by controlling transcription of peroxisomal fatty acid β-oxidation genes. RNAi knockdown, mutant analysis, RNA profiling, lipidomics PLoS genetics Medium 28273089
2017 Cancer-testis antigen HCA587/MAGEC2 directly interacts with TAF9 via a 9-amino acid transactivation domain motif; the interaction occurs in the nucleus and is confirmed by co-immunoprecipitation and GST pulldown; the conserved region of TAF9 is critical for HCA587/MAGEC2 binding. Co-immunoprecipitation (transfected and endogenous), GST pulldown, immunofluorescence co-localization Molecular medicine reports Low 29257297
2021 TAF9 is deacetylated by HDAC1; TAF9 overexpression increases fatty acid β-oxidation and reduces lipid droplet accumulation in NAFLD models; the DSS compound activates TAF9 via HDAC1-mediated deacetylation to confer protection against NAFLD. TAF9 overexpression/knockdown in vivo and in vitro, lipid droplet quantification, β-oxidation assay, pharmacological HDAC1 activation Frontiers in pharmacology Medium 34925033
2025 lncRNA938 directly binds TAF9 and regulates its nuclear localization; TAF9 activates TTK transcription via promoter binding; the lncRNA938–TAF9–TTK axis promotes EMT and hepatoblastoma progression. RNA immunoprecipitation, RNA pulldown, immunofluorescence (nuclear localization), luciferase reporter assay, Western blot, in vitro/in vivo functional assays Journal of translational medicine Medium 40841910

Source papers

Stage 0 corpus · 29 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 Human TAFII31 protein is a transcriptional coactivator of the p53 protein. Proceedings of the National Academy of Sciences of the United States of America 287 7761466
1998 A human SPT3-TAFII31-GCN5-L acetylase complex distinct from transcription factor IID. The Journal of biological chemistry 166 9726987
1998 The corepressor N-CoR and its variants RIP13a and RIP13Delta1 directly interact with the basal transcription factors TFIIB, TAFII32 and TAFII70. Nucleic acids research 114 9611234
1997 The class II trans-activator CIITA interacts with the TBP-associated factor TAFII32. Nucleic acids research 103 9171108
1995 Evolutionary conservation of human TATA-binding-polypeptide-associated factors TAFII31 and TAFII80 and interactions of TAFII80 with other TAFs and with general transcription factors. Proceedings of the National Academy of Sciences of the United States of America 75 7667268
2005 TAF9b (formerly TAF9L) is a bona fide TAF that has unique and overlapping roles with TAF9. Molecular and cellular biology 54 15899866
2000 Trichostatin A modulates expression of p21waf1/cip1, Bcl-xL, ID1, ID2, ID3, CRAB2, GATA-2, hsp86 and TFIID/TAFII31 mRNA in human lung adenocarcinoma cells. Biological chemistry 46 10746741
2002 Mdm-2 binding and TAF(II)31 recruitment is regulated by hydrogen bond disruption between the p53 residues Thr18 and Asp21. Oncogene 38 12370832
2001 Stabilization and activation of p53 by the coactivator protein TAFII31. The Journal of biological chemistry 38 11278372
2000 Robust mRNA transcription in chicken DT40 cells depleted of TAF(II)31 suggests both functional degeneracy and evolutionary divergence. Molecular and cellular biology 34 10866663
2017 Drosophila TRF2 and TAF9 regulate lipid droplet size and phospholipid fatty acid composition. PLoS genetics 32 28273089
2005 Characterization of hCINAP, a novel coilin-interacting protein encoded by a transcript from the transcription factor TAFIID32 locus. The Journal of biological chemistry 32 16079131
2015 p53 modulates the activity of the GLI1 oncogene through interactions with the shared coactivator TAF9. DNA repair 30 26282181
2012 TFIID TAF6-TAF9 complex formation involves the HEAT repeat-containing C-terminal domain of TAF6 and is modulated by TAF5 protein. The Journal of biological chemistry 24 22696218
2017 Histone deacetylase 1 activates PU.1 gene transcription through regulating TAF9 deacetylation and transcription factor IID assembly. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 19 28572446
2014 The TAF9 C-terminal conserved region domain is required for SAGA and TFIID promoter occupancy to promote transcriptional activation. Molecular and cellular biology 18 24550006
2005 TFIID and Spt-Ada-Gcn5-acetyltransferase functions probed by genome-wide synthetic genetic array analysis using a Saccharomyces cerevisiae taf9-ts allele. Genetics 18 16118188
2003 In vivo functional analysis of the histone 3-like TAF9 and a TAF9-related factor, TAF9L. The Journal of biological chemistry 15 12837753
2020 Human cytomegalovirus pp65 peptide-induced autoantibodies cross-reacts with TAF9 protein and induces lupus-like autoimmunity in BALB/c mice. Scientific reports 14 32541894
2006 Walleye dermal sarcoma virus retroviral cyclin directly contacts TAF9. Journal of virology 10 17035330
2014 E(y)1/TAF9 mediates the transcriptional output of Notch signaling in Drosophila. Journal of cell science 9 25015288
1997 Rat TAFII31 gene is induced upon programmed cell death in differentiated PC12 cells deprived of NGF. Biochemical and biophysical research communications 8 9168994
2022 Transcriptomic Analysis Reveals That Granulocyte Colony-Stimulating Factor Trigger a Novel Signaling Pathway (TAF9-P53-TRIAP1-CASP3) to Protect Retinal Ganglion Cells after Ischemic Optic Neuropathy. International journal of molecular sciences 6 35955492
1999 Repression of A TAF(II)32 isoform as part of a program of genes regulated during mpl ligand-induced megakaryocyte differentiation. Biochemical and biophysical research communications 5 10448067
2021 Cytomegalovirus-Associated Autoantibody against TAF9 Protein in Patients with Systemic Lupus Erythematosus. Journal of clinical medicine 4 34442018
2021 Activation of TAF9 via Danshensu-Induced Upregulation of HDAC1 Expression Alleviates Non-alcoholic Fatty Liver Disease. Frontiers in pharmacology 4 34925033
2017 Cancer‑testis antigen HCA587/MAGEC2 interacts with the general transcription coactivator TAF9 in cancer cells. Molecular medicine reports 4 29257297
2024 Taenia solium TAF6 and TAF9 bind to a downstream promoter element present in the Tstbp1 gene core promoter. PloS one 2 39208271
2025 LncRNA938/ TAF9/TTK axis promotes EMT and serves as a therapeutic target in hepatoblastoma. Journal of translational medicine 1 40841910

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