Affinage

BRF1

Transcription factor IIIB 90 kDa subunit · UniProt Q92994

Length
677 aa
Mass
73.8 kDa
Annotated
2026-06-09
65 papers in source corpus 36 papers cited in narrative 36 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

The BRF1 symbol in this corpus maps onto two distinct, internally coherent proteins, and the timeline cleanly separates them. The dominant entity is the RNA Polymerase III transcription factor BRF1 (TFIIIB90/hBRF, a TFIIB-related factor), a subunit of TFIIIB that recruits Pol III to its promoters (PMID:7995525, PMID:8943358). BRF1 is built as a bipartite, modular scaffold: its N-terminal TFIIB-homologous half carries the principal transcription-directing function and inserts into the Pol III active-site cleft, with the cyclin-repeat subdomain contacting the Pol III subunit C34, while its C-terminal half assembles TFIIIB on DNA by providing the binding surfaces for TBP and Bdp1 (PMID:9710642, PMID:24277937). BRF1 binds TBP through a bipartite, multi-site interface on the first TBP repeat that overlaps the surface used by Pol II factors, and it acts in concert with its TFIIB-homology domain to dissociate TBP dimers and dramatically stabilize the TBP–Bdp1 interaction (PMID:8662956, PMID:9488486, PMID:15190063); a 66-residue C-terminal segment serves as a two-sided adhesive that anchors Bdp1 via its conserved SANT domain (PMID:16551611, PMID:19086269). BRF1 is recruited into the TFIIIB–TFIIIC–DNA complex through multiple peptide contacts with the TPR repeats of the TFIIIC subunit Tfc4, an interaction subject to Tfc4 autoinhibition that is relieved by conformational change (PMID:12930823, PMID:16880507). Distinct human BRF1 splice variants confer promoter-type specificity, functioning at gene-internal tRNA-type promoters while a separate variant serves the U6-type promoter (PMID:8943358, PMID:10921893). BRF1 expression and activity are heavily regulated: it is repressed by Maf1 and during p53-mediated arrest, ubiquitinated by RNF12, and transcriptionally driven by c-Jun, Sp1, and ERα to tune Pol III output (PMID:11283026, PMID:17505538, PMID:30413534, PMID:32115405, PMID:28972307). Biallelic activity-reducing BRF1 mutations cause cerebellar hypoplasia and intellectual disability, and Brf1 is essential for blastocyst viability and tissue homeostasis in mice (PMID:25561519, PMID:30858608). The second, unrelated protein sharing the BRF1 name is the ARE-binding zinc-finger mRNA decay factor (ZFP36L1/TIS11b), which destabilizes ARE-containing mRNAs by recruiting deadenylation, decapping, and exonucleolytic decay enzymes through two activation domains and delivering transcripts to processing bodies (PMID:12198173, PMID:15687258, PMID:17369404); its decay activity is suppressed by PKB phosphorylation at S92/S203 driving 14-3-3 sequestration and by MK2, while PKA phosphorylation at S334 switches its association between Dcp1a and Cnot1, and it acts downstream of FGF/ERK to destabilize Nanog mRNA and limit pluripotency (PMID:15538381, PMID:17030608, PMID:18326031, PMID:27708140, PMID:24733888).

Mechanistic history

Synthesis pass · year-by-year structured walk · 26 steps
  1. 1994 High

    Establishing the molecular partners of BRF defined it as the bridging subunit of TFIIIB, answering how Pol III machinery is tethered to TBP and TFIIIC.

    Evidence Protein-protein binding assays of BRF fragments with TFIIIC, TBP and Pol III subunit C34 in yeast

    PMID:7995525

    Open questions at the time
    • Did not resolve the bipartite vs single-site nature of TBP binding
    • No structural model of the contacts
  2. 1996 High

    Purification of human BRF1 as a TBP-associated factor and its immunodepletion established that hBRF is required specifically for gene-internal (tRNA-type) but not TATA-type Pol III promoters.

    Evidence Biochemical purification, cloning, and immunodepletion followed by in vitro transcription from VAI and U6 promoters

    PMID:8943358

    Open questions at the time
    • Did not explain the molecular basis of promoter-type discrimination
    • Identity of the U6-specific factor unresolved at this point
  3. 1996 High

    Reconstitution from recombinant subunits showed BRF1 enhances the weak TBP–Bdp1 interaction >25-fold and that BRF1/Bdp1 occupy TBP surfaces shared with Pol II factors, defining BRF1 as the assembly nucleator of TFIIIB.

    Evidence Recombinant TFIIIB reconstitution, quantitative binding assays, and competition with TFIIA/TFIIB

    PMID:8662956

    Open questions at the time
    • Precise residues on TBP not yet mapped
    • Stoichiometry and kinetics of assembly not fully defined
  4. 1997 High

    Deletion analysis revealed functional complementarity between the BRF1 and Bdp1 subunits, showing the C-terminal half alone supports TBP/Bdp1 binding and complex assembly independent of the TFIIB-homology domain.

    Evidence N-terminal deletion series tested in TFIIIB-DNA assembly and TFIIIC-independent in vitro transcription

    PMID:9271407

    Open questions at the time
    • Did not assign specific transcription steps to the N-terminal domain
    • Mechanism of subunit reciprocity left open
  5. 1998 High

    Systematic mutagenesis of TBP and dissection of BRF1 fragments defined the modular architecture: TBP binding maps to a defined surface on the first repeat, assembly function to a C-proximal segment, and transcription-directing function to the N-terminal TFIIB-homology half.

    Evidence 91 TBP surface mutants in gel-shift and transcription assays; BRF fragment library with footprinting and protein-DNA cross-linking

    PMID:9488486 PMID:9710642

    Open questions at the time
    • High-resolution structure of the contacts still lacking
    • How the two halves cooperate during initiation not resolved
  6. 2000 High

    Demonstration that BRF1 partners with TRF1 rather than TBP in Drosophila, and that splice variants confer distinct promoter specificity in human, established context-dependent flexibility of BRF1-containing TFIIIB complexes.

    Evidence IP, immunodepletion/reconstitution, and polytene colocalization in fly; isoform cDNA isolation and promoter-specific in vitro transcription in human

    PMID:10850489 PMID:10921893

    Open questions at the time
    • Determinants of TBP-vs-TRF1 selection not defined
    • Structural basis of promoter discrimination by isoforms unresolved
  7. 2000 High

    Recombinant BRF1+TBP over the SNR6 TATA box sufficed to direct Ty3 integration, showing the minimal TFIIIB scaffold positions both Pol III initiation and retroviral integration machinery.

    Evidence In vitro integration assay with recombinant BRF1 and TBP in a TFIIIC-independent system

    PMID:10882723

    Open questions at the time
    • Generality beyond SNR6/TATA promoters not tested
    • Physical link to integrase not mapped
  8. 2001 Medium

    Linking human BRF1 (TAF3B2) protein stability to p53-mediated arrest established control of Pol III capacity through regulated BRF1 abundance.

    Evidence Complementation with in vitro transcription and protein stability analysis in p53-arrested cells

    PMID:11283026

    Open questions at the time
    • Degradation pathway not identified at this stage
    • Direct vs indirect p53 effect unresolved
  9. 2002 High

    Identification of a distinct ARE-binding zinc-finger BRF1 (ZFP36L1) via genetic rescue established a completely separate protein that actively drives ARE-dependent mRNA decay and antagonizes PI3K-mediated stabilization.

    Evidence Retroviral cDNA rescue of decay-deficient cells, siRNA knockdown, and zinc-finger mutagenesis

    PMID:12198173

    Open questions at the time
    • Decay enzymes recruited not yet identified
    • Relationship to the Pol III BRF1 is purely nominal (name collision)
  10. 2002 Medium

    Discovery of the PCF1-1 gain-of-function mutation in Tfc4 showed BRF1 recruitment is gated by Tfc4 autoinhibition that can be relieved by conformational change.

    Evidence Site-directed mutagenesis, modeling, and affinity assays for BRF1 and Bdp1 with TFIIIC131 fragments

    PMID:12167707

    Open questions at the time
    • BRF1 does not bind at the mutation site — conformational mechanism inferred not directly observed
    • Structural state of relieved autoinhibition not solved
  11. 2003 High

    Mapping overlapping BRF1 and Bdp1 binding sites on Tfc4 TPRs explained how the two TFIIIB subunits are competitively recruited onto the TFIIIC scaffold.

    Evidence Mutagenesis of Tfc4 TPR residues with assembly and direct binding assays plus multicopy suppression

    PMID:12930823

    Open questions at the time
    • Order of recruitment during assembly not fully resolved
    • Structure of the Tfc4-BRF1 interface lacking
  12. 2004 High

    PKB phosphorylation of the ARE-decay BRF1 at S92 and demonstration of BRF1-driven TBP dimer dissociation in the transcription protein together defined active regulatory mechanisms in both namesake proteins.

    Evidence In vitro decay/kinase assays, S92A mutagenesis and 14-3-3 co-IP (ZFP36L1); in vitro TBP dimerization assays with domain fragments (Pol III BRF1)

    PMID:15190063 PMID:15538381

    Open questions at the time
    • Whether a second phospho-site cooperates with S92 not yet known
    • Structural basis of dimer dissociation not determined
  13. 2005 High

    Defining two activation domains on ARE-decay BRF1 that recruit deadenylation, decapping and exonucleolytic enzymes established it as a modular platform for assembling the mRNA decay machinery; engineering a BRF1-TBP triple fusion confirmed the modular bipartite TBP-interaction mode of the Pol III BRF1.

    Evidence Co-IP of decay enzymes, tethering and dominant-negative assays (ZFP36L1); triple-fusion reconstitution with footprinting and in vivo complementation (Pol III BRF1)

    PMID:15687258 PMID:16227432

    Open questions at the time
    • Direct vs indirect contact of each decay enzyme not all resolved
    • Bdp1-independent recruitment in fusion vs native context differences
  14. 2006 High

    Residue-level mapping of the BRF1–Bdp1 interface (66-aa two-sided adhesive engaging the Bdp1 SANT domain) and demonstration of a second PKB site (S203) cooperating with S92 in the decay protein refined the molecular models for both proteins.

    Evidence Mutagenesis/cross-linking of BRF1-Bdp1 segments (Pol III); kinase, mutagenesis, fractionation and KO-cell stability assays for S92/S203 14-3-3 sequestration (ZFP36L1); genome-wide ChIP of TRF1/BRF in fly

    PMID:16551611 PMID:17030608 PMID:17170711

    Open questions at the time
    • Atomic structure of the BRF1-Bdp1 interface not yet at NMR resolution here
    • Genome-wide BRF1 targets in mammals not defined
  15. 2007 Medium

    Placing Maf1 repression directly through BRF1/Brf2 and showing ARE-decay BRF1 delivers mRNAs to processing bodies positioned both proteins within their respective regulatory pathways.

    Evidence Pol III luciferase reporter epistasis (Maf1); siRNA depletion, dominant-negative, tethering and live imaging of ARE-mRNAs in PBs

    PMID:17369404 PMID:17505538

    Open questions at the time
    • Direct Maf1-BRF1 contact not biochemically mapped here
    • PB localization step relative to decay completion not fully ordered
  16. 2008 High

    MK2 phosphorylation of ARE-decay BRF1 at S54/S92/S203 inhibits decay downstream of RNA binding and enzyme recruitment, distinguishing the regulatory step from substrate engagement.

    Evidence In vitro kinase, site-directed mutagenesis, decay assays, ARE binding and decay-enzyme co-IP

    PMID:18326031

    Open questions at the time
    • Identity of the C-terminal MK2 site not determined
    • Mechanism downstream of recruitment that blocks decay unresolved
  17. 2008 High

    NMR mapping localized the principal BRF1 anchorage on the convex SANT-domain surface of Bdp1 (residues 470–495 of BRF1), giving a residue-resolution model of the TFIIIB core interface.

    Evidence NMR chemical shift perturbation with minimal functional Brf1/Bdp1 segments

    PMID:19086269

    Open questions at the time
    • Full-length complex structure not solved
    • DNA-bound conformation of the interface not captured
  18. 2010 Medium

    Identifying c-Jun/JNK1 induction of BRF1 and TBP expression connected Pol III transcriptional capacity to stress and ethanol signaling at the level of TFIIIB abundance.

    Evidence ChIP of c-Jun at the BRF1 promoter, reporters, siRNA, and an in vivo mouse alcohol model

    PMID:21106530

    Open questions at the time
    • Direct enzymatic link from JNK1 to BRF1 promoter not isolated
    • Physiological consequence of elevated Pol III output not defined
  19. 2011 Medium

    Demonstration that the ARE-decay BRF1 (Tis11b) represses Dll4 by interfering with 3'-end cleavage/polyadenylation extended its repertoire beyond classical decay into co-transcriptional/processing control.

    Evidence siRNA, RNA-IP of endogenous Dll4 mRNA, 3'-UTR reporters and poly(A) site usage analysis

    PMID:21832157

    Open questions at the time
    • Generality across other targets not established
    • Mechanistic link to the cleavage/polyadenylation machinery not mapped
  20. 2013 High

    Site-specific cross-linking in the native preinitiation complex mapped the full BRF1 interaction network, showing the N-terminal domain behaves like TFIIB in the Pol III cleft and contacts C34, while the C-terminal domain holds TBP and Bdp1 on the promoter.

    Evidence Non-natural amino acid cross-linking and hydroxyl radical probing in the Pol III PIC

    PMID:24277937

    Open questions at the time
    • Dynamic transitions during open-complex formation not captured
    • Quantitative contributions of each contact to initiation not measured
  21. 2014 Medium

    Positioning ARE-decay BRF1 downstream of FGF/ERK to destabilize Nanog mRNA established a signaling-to-mRNA-decay axis controlling pluripotency and lineage commitment.

    Evidence FGF/ERK manipulation with Brf1 gain/loss-of-function and mRNA stability/differentiation assays in mESCs

    PMID:24733888

    Open questions at the time
    • Direct vs indirect ERK control of Brf1 not fully separated
    • Full target set beyond Nanog not catalogued
  22. 2015 High

    Identifying biallelic activity-reducing BRF1 mutations that lower tRNA-gene occupancy and Pol III transcription, with cross-species recapitulation, established BRF1 loss-of-function as the cause of cerebellar hypoplasia and intellectual disability.

    Evidence Exome sequencing, yeast complementation with disease alleles, ChIP occupancy, in vitro Pol III transcription, and zebrafish CRISPR/morpholino

    PMID:25561519

    Open questions at the time
    • Tissue-specific basis of the neurodevelopmental phenotype not resolved
    • Which Pol III transcripts drive pathology not pinpointed
  23. 2016 High

    Showing PKA phosphorylation of ARE-decay BRF1 at S334 switches its association between Dcp1a and Cnot1 revealed phosphorylation-driven routing between distinct decay pathways and stabilization of the protein.

    Evidence Kinase assays, phosphomimetic mutagenesis, half-life measurement and co-IP with Dcp1a and Cnot1

    PMID:27708140

    Open questions at the time
    • Physiological signals driving S334 phosphorylation in vivo not defined
    • Net effect on specific endogenous targets not mapped
  24. 2018 Medium

    Identifying RNF12-mediated K27/K33-linked ubiquitination of Pol III BRF1 and the Rpc82 WH3 contact within the PIC added a degradative regulatory input and a new Pol III subunit contact to the transcription-factor BRF1.

    Evidence Co-IP, in vitro ubiquitination with linkage analysis and Pol III/proliferation assays (RNF12); site-specific photo-crosslinking with functional assays (Rpc82)

    PMID:29177422 PMID:30413534

    Open questions at the time
    • Whether K27/K33 chains target BRF1 for degradation or signaling unresolved
    • Functional consequence of the Rpc82 WH3-BRF1 contact for initiation not quantified
  25. 2019 High

    Conditional and constitutive Brf1 knockout in mice established that the Pol III transcription factor is essential for blastocyst viability and adult tissue homeostasis, with loss inducing apoptosis rescuable by re-expression.

    Evidence Conditional KO mouse models, genetic rescue, histology and apoptosis assays

    PMID:30858608

    Open questions at the time
    • Tissue-specific transcript dependencies not defined
    • Threshold of Pol III activity for survival not determined
  26. 2020 Medium

    Showing Sp1 and ERα drive BRF1 expression and promoter occupancy connected upstream Pol II transcription factors to the regulation of Pol III capacity through BRF1 abundance.

    Evidence Reporter assays, ChIP of Sp1/TBP/TFIIAα/p300 at the BRF1 promoter, and knockdown/overexpression (Sp1); co-IP, colocalization and ChIP with siRNA/tamoxifen (ERα)

    PMID:28972307 PMID:32115405

    Open questions at the time
    • Direct functional consequence of ERα-BRF1 physical interaction beyond expression unclear
    • Crosstalk between Sp1- and ERα-driven control not integrated

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the bipartite BRF1 contacts are dynamically remodeled during Pol III open-complex formation and promoter escape, and the full in vivo target spectrum and tissue-specific essential transcripts underlying BRF1-related disease are uncharacterized.
  • No cryo-EM/structural snapshot of dynamic initiation states in the corpus
  • Tissue-specific Pol III transcript dependencies driving disease undefined
  • Integration of the two namesake proteins (if any biological overlap) not addressed

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0140110 transcription regulator activity 4 GO:0003723 RNA binding 3 GO:0003677 DNA binding 2 GO:0140223 general transcription initiation factor activity 2
Localization
GO:0000228 nuclear chromosome 2 GO:0005634 nucleus 2
Pathway
R-HSA-74160 Gene expression (Transcription) 4 R-HSA-8953854 Metabolism of RNA 3
Partners
BDP1C34CNOT1DCP1AESR1RNF12TBPTFC4
Complex memberships
Pol III preinitiation complexTFIIIB

Evidence

Reading pass · 36 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1994 Yeast BRF (BRF1 ortholog) binds the 135-kD subunit of TFIIIC and also binds TBP; TBP interacts with both the TFIIB-homologous N-terminal half and the C-terminal half of BRF, with two conserved C-terminal regions required for the TBP–BRF C-terminal interaction. BRF also binds RNA Pol III subunit C34, and a region of C34 necessary for this interaction was defined. Protein–protein interaction assays (binding assays between BRF fragments and TFIIIC subunit, TBP, and Pol III subunit C34); functional analysis of deletion mutants; TBP mutants that selectively inhibit Pol III transcription in vivo impair the BRF C-terminal–TBP interaction Genes & development High 7995525
1996 Human BRF1 (TFIIIB90/hBRF, 88 kDa) was purified as a TBP-associated complex and identified as the human homolog of yeast BRF. Immunodepletion of hBRF severely debilitates transcription from the tRNA-type VAI promoter but does not affect transcription from the TATA box-containing human U6 promoter, indicating promoter-type-specific requirement for hBRF. Biochemical purification; cDNA cloning; immunodepletion of hBRF from transcription extracts followed by in vitro transcription from VAI and U6 promoters Molecular and cellular biology High 8943358
1996 Yeast TFIIIB90 (Bdp1/B") interacts weakly with TBP alone but this interaction is enhanced at least 25-fold by BRF1. TFIIIB was reconstituted from recombinant subunits (TBP, BRF1, TFIIIB90). Binding sites for BRF1 and TFIIIB90 on TBP-DNA overlap with binding sites for TFIIA and TFIIB, indicating shared TBP interface. Recombinant protein reconstitution; in vitro binding assays; competition with Pol II factors TFIIA and TFIIB The Journal of biological chemistry High 8662956
1997 N-terminal deletion analysis of yeast Brf1 showed that the C-terminal half (residues 317–596) lacking the entire TFIIB-homologous domain can still interact with DNA-bound TBP and with B"/Bdp1. Brf1(165–596) lacking 164 N-proximal TFIIB-homologous residues is competent for TFIIIB-DNA complex assembly and TFIIIC-independent transcription, revealing functional complementarity and reciprocity between Brf1 and B" subunits. N-terminal deletion series of Brf1 tested in TFIIIB-DNA complex assembly and in vitro transcription; genetic complementation assays Molecular and cellular biology High 9271407
1998 TBP surface residues on the top and side of the first TBP repeat (K181, L185, R186, E206, R231, L232, R235, K236, R239, Q242, K243, K249, F250) are required for interaction with yeast Pol III TAF Brf. The Brf C-terminal fragment (lacking TFIIB-homology region) retains TBP-DNA binding via this same surface. Brf and TFIIB interact differently with TBP; the Brf-binding surface on TBP overlaps with surfaces required for activated Pol II transcription. 91 human TBP surface mutants analyzed in gel-shift assays with purified Brf and B"; in vitro U6 snRNA transcription; equivalent yeast TBP mutations tested Molecular and cellular biology High 9488486
1998 Systematic analysis of Brf fragments defined that the principal TFIIIB-assembly function maps to a C-proximal segment (aa 435–545), while the principal transcription-directing function resides in the N-proximal TFIIB-homologous half. Split Brf fragments (aa 1–282 + 284–596) reconstitute fully active TFIIIB-DNA complexes. Photochemical cross-linking mapped proximities of each Brf half to DNA, providing a global model of Brf domain organization in the TFIIIB-DNA complex. Systematic Brf fragment analysis; in vitro transcription reconstitution; in vitro footprinting; photochemical protein-DNA cross-linking; TBP interaction mapping Molecular and cellular biology High 9710642
2000 In Drosophila, TRF1 (rather than TBP) forms a complex with BRF to direct RNA polymerase III transcription. Immunoprecipitation showed TRF1:BRF complex in vivo; immunodepleted extracts supplemented with recombinant TRF1 and BRF reconstitute transcription of tRNA, 5S, and U6 RNA genes. In vivo, the majority of TRF1 is complexed with BRF and the two proteins colocalize at many polytene chromosome sites containing RNA Pol III genes. Immunoprecipitation; immunodepletion followed by in vitro transcription reconstitution with recombinant proteins; immunofluorescence colocalization on polytene chromosomes Cell High 10850489
2000 Recombinant Brf and TBP subunits of TFIIIB, interacting over the SNR6 TATA box, are sufficient to direct Ty3 retrotransposon integration at the SNR6 transcription initiation site in the absence of detectable TFIIIC or TFIIIB subunit B", establishing that the minimal requirements for Pol III transcription and Ty3 integration are very similar. In vitro integration assay with recombinant Brf and TBP; TFIIIC-independent system using U6/SNR6 gene with TATA box The Journal of biological chemistry High 10882723
2000 Alternatively spliced human BRF variants have distinct promoter specificities: hBRF1 functions at the gene-internal 5S, VA1, 7SL and EBER2 promoters, while a different variant hBRF2 is required at the gene-external human U6 promoter, demonstrating that Pol III utilizes different TFIIIB complexes at structurally distinct promoters. Isolation of alternatively spliced cDNAs; immunopurification of hBRF-containing complexes; in vitro transcription from different Pol III promoter types The EMBO journal High 10921893
2001 In human cells, a TFIIIB subcomponent containing TBP and TAF3B2 (human BRF1) is the target of repression during p53-mediated cell cycle arrest. TAF3B2 protein levels are markedly reduced in extracts from cell cycle-arrested cells due to decreased TAF3B2 protein stability, providing a mechanism for reducing Pol III transcriptional capacity. Cell-based complementation assays with in vitro transcription; protein stability analysis in p53-arrested cells; cell fractionation The Journal of biological chemistry Medium 11283026
2002 BRF1 (butyrate response factor 1, ZFP36L1 family) was identified as an essential regulator of ARE-dependent mRNA decay: a mutagenized cell line (slowC) failing to degrade ARE-containing mRNA carries frameshift mutations in both BRF1 alleles; retroviral re-expression rescues rapid mRNA decay. siRNA knockdown independently confirms BRF1's active role. BRF1 accelerates mRNA decay and antagonizes PI3-kinase-mediated stabilization; zinc finger mutations abolish both ARE binding and mRNA decay activity. Functional genetic screen (retroviral cDNA library rescue of decay-deficient cells); flow cytometry-based reporter assay; siRNA knockdown; transfection of BRF1 zinc finger mutants The EMBO journal High 12198173
2002 A gain-of-function mutation (PCF1-1, H190Y) in TPR2 of TFIIIC131 increases binding affinity of TFIIIC131 for Brf1 without affecting Bdp1 binding affinity, by overcoming autoinhibition of Brf1 binding—Brf1 does not interact directly at the mutation site, but the mutation stabilizes an alternative conformation of TFIIIC131 that promotes Brf1 interaction. Site-directed mutagenesis; structural modeling; binding affinity assays for Brf1 and Bdp1 with TFIIIC131 fragments; dominant mutation analysis Molecular and cellular biology Medium 12167707
2003 The Brf1 and Bdp1 subunits of TFIIIB bind to overlapping sites in the tetratricopeptide repeats (TPRs) of Tfc4 (TFIIIC subunit). TPRs6–9 contain a binding site for Brf1; the L469K mutation in TPR7 reduces Brf1 recruitment into TFIIIB-TFIIIC-DNA complexes and reduces direct Tfc4–Brf1 interaction, and also decreases Bdp1 incorporation, indicating both subunits compete for overlapping Tfc4 sites. Site-directed mutagenesis of Tfc4 TPR residues; biochemical assembly assays for TFIIIB-TFIIIC-DNA complexes; direct binding assays; multicopy suppression analysis The Journal of biological chemistry High 12930823
2004 Protein kinase B (PKB/Akt) phosphorylates BRF1 (ARE-decay factor) at serine 92 (S92), which impairs BRF1 mRNA decay activity without affecting ARE binding, and induces complex formation of BRF1 with the scaffold protein 14-3-3, causing ARE-mRNA stabilization. Recombinant BRF1 in vitro mRNA decay assay; in vitro PKB kinase assay; phosphorylation-site mutagenesis (S92A); co-immunoprecipitation of BRF1 with 14-3-3; ARE-mRNA stability measurements in vivo The EMBO journal High 15538381
2004 Brf1 (yeast) induces dissociation of TBP dimers, requiring both its high-affinity TBP-binding C-terminal domain and its TFIIB homology domain working in concert; the C-terminal TBP-binding domain alone is insufficient to promote TBP dimer dissociation. In vitro TBP dimerization and dissociation assays with Brf1 domain fragments; functional domain analysis The Journal of biological chemistry Medium 15190063
2005 TTP and BRF-1 (ARE-decay factors) each contain two activation domains that recruit mRNA decay enzymes involved in deadenylation, decapping, 3'-to-5' exonucleolytic decay, and 5'-to-3' exonucleolytic decay. The N-terminal activation domain of BRF-1 functions as a binding platform for mRNA decay enzymes. Both activation domains can activate mRNA decay when fused to a heterologous RNA-binding protein and inhibit ARE-mediated mRNA decay when overexpressed. Co-immunoprecipitation of mRNA decay enzymes with TTP/BRF-1; tethering assays (fusion to heterologous RNA-binding protein); dominant-negative overexpression; two activation domain mapping Genes & development High 15687258
2005 A Brf1-TBP triple fusion protein (TBP core placed between N- and C-proximal domains of Brf1) effectively replaces both Brf1 and TBP in TFIIIC-dependent and -independent transcription in vitro, forms extremely stable TFIIIB-DNA complexes, and can recruit Pol III for TATA box-directed transcription in the absence of Bdp1, confirming the modular architecture of Brf1 and its bipartite TBP interaction mode. Structure-informed protein engineering (triple fusion); in vitro transcription reconstitution; chemical nuclease footprinting; in vivo complementation in yeast Proceedings of the National Academy of Sciences of the United States of America High 16227432
2006 PKB phosphorylates BRF1 (ARE-decay factor) at a second regulatory site, S203, which cooperates with S92 in vivo. Double alanine mutation of both S92 and S203 uncouples BRF1 from PKB regulation, leading to constitutive mRNA decay. Phosphorylation-dependent 14-3-3 binding requires phosphorylation at both sites. BRF1 is subject to proteasomal degradation (half-life <3 h) but phosphorylation stabilizes it; cell compartment fractionation showed that 14-3-3 binding sequesters BRF1 through relocalization, preventing mRNA decay activity and protecting from proteasomal degradation. In vitro kinase assay; site-directed mutagenesis (S92A, S203A, double mutant); mRNA decay assays; co-immunoprecipitation with 14-3-3; protein stability assays in PKBα−/− cells; cell fractionation Molecular and cellular biology High 17030608
2006 The principal attachment site of Brf1 for Bdp1 in TFIIIB was mapped: a 66-amino acid segment of Brf1's C-terminal half serves as a two-sided adhesive surface with one face interacting with TBP and the other anchoring Bdp1. The interacting Bdp1 domain was demarcated to a 66-amino acid segment including the SANT domain, which is the most phylogenetically conserved region of Bdp1. Structure-informed site-directed mutagenesis; photochemical protein-DNA cross-linking; deletion series of Brf1 and Bdp1 fragments in binding assays The Journal of biological chemistry High 16551611
2006 Brf1 peptides from three distinct regions interact with the TPR-containing Tfc4 subunit of TFIIIC. A peptide binding specifically to TPR6-9 of Tfc4 promotes formation of TFIIIC-DNA and Brf1-TFIIIC-DNA complexes and causes a conformational change in TFIIIC that overcomes Tfc4 autoinhibition of Brf1 binding, suggesting repositioning of Brf1 is required during TFIIIB assembly. Yeast two-hybrid screen of Brf1 peptide libraries against Tfc4 fragments; native gel mobility shift assays; biochemical binding studies Molecular and cellular biology Medium 16880507
2006 In Drosophila, genome-wide ChIP analysis identified 354 TRF1-binding sites, ~78% of which colocalize with BRF. The TRF1/BRF complex is functionally required for transcription of novel targets including 7SL RNA and small nucleolar RNAs, indicating TRF1/BRF is responsible for all known classes of Pol III transcription in Drosophila. Genome-wide ChIP with tiling microarrays; functional transcription assays for novel targets The EMBO journal Medium 17170711
2007 Human Maf1 represses RNA Pol III transcription via direct interaction with TFIIIB, specifically through the TFIIB family members Brf1 and Brf2 (not through other components). This was demonstrated in vivo with a Pol III luciferase reporter assay. RNA Pol III luciferase reporter assay in vivo; epistasis analysis showing Maf1 repression acts through Brf1 and Brf2 subunits of TFIIIB International journal of biological sciences Medium 17505538
2007 TTP and BRF-1 (ARE-binding proteins) deliver ARE-mRNAs to processing bodies (PBs). Depletion of endogenous TTP and BRF proteins or dominant-negative TTP impairs ARE-mRNA localization to PBs. TTP and BRF-1 can tether mRNAs to PBs and TTP can nucleate PB formation on untranslated mRNAs. ARE-mRNA PB localization is mediated by TTP N- and C-terminal domains and occurs downstream from polysome release. siRNA depletion of TTP and BRF proteins; dominant-negative overexpression; tethering assays; fluorescence microscopy/live imaging of reporter ARE-mRNAs in PBs; cycloheximide treatment to trap polysomes Genes & development High 17369404
2008 MAPK-activated protein kinase 2 (MK2) phosphorylates BRF1 (ARE-decay factor) at S54, S92, S203, and an unidentified C-terminal site, inhibiting BRF1's ARE mRNA decay activity. MK2-mediated inhibition requires phosphorylation at S54, S92, and S203. Phosphorylation by MK2 does not alter BRF1's ability to bind AREs or associate with mRNA decay enzymes, suggesting inhibition occurs downstream of RNA binding and decay enzyme recruitment. In vitro kinase assays with MK2 and BRF1 fragments; site-directed mutagenesis (S54, S92, S203); ARE-mRNA decay assays in cells with active MK2; ARE-binding and co-immunoprecipitation of decay enzymes RNA (New York, N.Y.) High 18326031
2008 NMR mapping of the Brf1–Bdp1 interaction at single-amino acid resolution showed that the principal anchorage site of Brf1 is on a convex surface of Bdp1 encompassing helix 1 and helix 3 of its conserved SANT domain, with the main Bdp1 anchorage provided by residues 470–495 of Brf1. NMR chemical shift perturbation mapping using minimal functional segments of Brf1 and Bdp1; NMR-derived structural model Biochemistry High 19086269
2010 Ethanol induces RNA Pol III-dependent transcription in HepG2 cells and primary mouse hepatocytes by upregulating BRF1 and TBP expression (TFIIIB components) through JNK1 activation and enhanced c-Jun expression. c-Jun is directly recruited to TBP, BRF1, and tRNA gene promoters. Chronic alcohol administration in mice increases BRF1, TBP, tRNA, and 5S rRNA transcription in liver. Chromatin immunoprecipitation (ChIP); luciferase reporter assays; siRNA knockdown; in vivo mouse alcohol feeding model; quantitative RT-PCR The Journal of biological chemistry Medium 21106530
2011 Tis11b/BRF1 (ARE-decay factor) binds to endogenous Dll4 mRNA and represses its expression without affecting mRNA stability, through a novel mechanism involving mRNA 3'-end processing. One AUUUA motif in a weak noncanonical polyadenylation signal in the Dll4 3'-UTR is the major Tis11b-binding site. Inhibition of Tis11b expression changes the ratio between mRNAs cleaved or read-through at the poly(A) signal, indicating Tis11b interferes with mRNA cleavage and polyadenylation efficiency. siRNA knockdown of Tis11b in endothelial cells; RNA immunoprecipitation of endogenous Dll4 mRNA; 3'-UTR reporter assays; poly(A) site usage analysis; hypoxia treatment Molecular biology of the cell Medium 21832157
2013 Site-specific non-natural amino acid cross-linking mapped Brf1's protein interaction network in the Pol III preinitiation complex: the N-terminal domain of Brf1 shows multiple protein interactions in the Pol III active-site cleft reminiscent of TFIIB, with the cyclin repeat subdomain additionally contacting C34 at its WH2–WH3 connecting region. The C-terminal domain of Brf1 contains extensive binding sites for TBP and Bdp1 to hold TFIIIB together on the promoter. Site-specific non-natural amino acid incorporation for cross-linking; site-directed hydroxyl radical probing; protein interaction mapping in the preinitiation complex Molecular and cellular biology High 24277937
2014 Brf1 (ZFP36L1/mRNA decay factor) operates downstream of FGF/ERK MAP kinase signaling in mouse embryonic stem cells: ERK signaling upregulates Brf1, which directly destabilizes target mRNAs including Nanog mRNA to disrupt pluripotency-associated gene expression and attenuate mESC self-renewal. Enhanced Brf1 expression preferentially regulates mesendoderm commitment during differentiation, accelerating primitive streak marker expression. FGF/ERK pathway manipulation; Brf1 gain-of-function and loss-of-function in mESCs; mRNA stability assays for Nanog and other targets; differentiation assays Proceedings of the National Academy of Sciences of the United States of America Medium 24733888
2015 Biallelic missense mutations in BRF1 reduce Brf1 occupancy at tRNA target genes in S. cerevisiae, impair yeast cell growth, and reduce Pol III-related transcription activity in vitro. CRISPR-mediated deletion of brf1 in zebrafish recapitulates neurodevelopmental phenotypes. In vivo complementation showed all four candidate disease mutations to be pathogenic in an isoform-specific context, confirming BRF1 mutations that reduce protein activity cause cerebellar hypoplasia and intellectual disability. Whole-exome sequencing; yeast complementation with human BRF1 disease alleles; ChIP for Brf1 occupancy at tRNA genes in yeast; in vitro Pol III transcription assay; CRISPR deletion and morpholino knockdown in zebrafish Genome research High 25561519
2016 TIS11b/BRF1 (ARE-decay factor) is phosphorylated by PKA at S54 and S334. Phosphomimetic mutation at C-terminal S334 markedly increases TIS11b half-life and enhances mRNA decay activity; this is accompanied by enhanced interaction with the decapping coactivator Dcp1a. Prevention of phosphorylation at S334 potentiates interaction with the Ccr4-Not deadenylase complex subunit Cnot1, revealing that differential phosphorylation at S334 switches TIS11b's association between distinct decay pathway components. Site-directed mutagenesis; in vitro kinase assays; phosphosite-specific immunodetection; protein half-life measurements; co-immunoprecipitation with Dcp1a and Cnot1; mRNA decay assays Molecular biology of the cell High 27708140
2017 BRF1 (TFIIIB subunit) physically interacts with estrogen receptor alpha (ERα) in breast cancer cells, as shown by co-immunoprecipitation and colocalization in the nucleus. ERα mediates BRF1 expression, and BRF1 and ERα synergistically regulate transcription of Pol III genes. Inhibition of ERα by siRNA or tamoxifen reduces BRF1 levels and Pol III gene expression. Co-immunoprecipitation; immunofluorescence colocalization; ChIP; siRNA knockdown of ERα; tamoxifen treatment; Pol III gene expression analysis Molecular oncology Medium 28972307
2018 RNF12, a RING domain-containing ubiquitin E3 ligase, physically interacts with BRF1 (TFIIIB subunit) and catalyzes Lys27- and Lys33-linked polyubiquitination of BRF1. RNF12 negatively regulates Pol III-dependent transcription and cell proliferation via BRF1. Co-immunoprecipitation; in vitro ubiquitination assay; linkage-specific ubiquitin chain analysis; Pol III transcription assays; cell proliferation assays with RNF12 overexpression/knockdown The Journal of biological chemistry Medium 30413534
2018 The WH3 insertion domain of Rpc82 (TFIIE-related Pol III subunit) interacts with BRF1 within the preinitiation complex, as revealed by site-specific photo-crosslinking. Rpc82 also contacts upstream DNA and the protrusion and wall domains of the Pol III cleft, with the WH3 insertion important for cell growth and in vitro transcription activity. Site-specific photo-crosslinking with non-natural amino acid; hydroxyl radical probing; in vitro transcription assays; genetic growth assays Nucleic acids research Medium 29177422
2019 Brf1 knockout in mice leads to embryonic lethality at the blastocyst stage. Conditional deletion of Brf1 in gastrointestinal epithelial tissues (intestine, liver, pancreas) is incompatible with organ homeostasis and induces apoptosis. Overexpression of BRF1 rescues the phenotypes of Brf1 deletion in intestine and liver, confirming BRF1 is essential for normal tissue homeostasis. Conditional knockout mouse models; genetic rescue by BRF1 overexpression; histological analysis; apoptosis assays Cell death and differentiation High 30858608
2020 Sp1 controls BRF1 expression by binding to the BRF1 promoter 4 (BRF1P4) and promoting occupancy of TBP, TFIIAα, and p300 at this promoter, thereby modulating Pol III gene transcription. Sp1 knockdown inhibits BRF1 expression and Pol III transcription; Sp1 overexpression enhances these activities. Reporter gene assays; ChIP for Sp1, TBP, TFIIAα, p300 at BRF1 promoter; siRNA knockdown and overexpression of Sp1; Pol III transcription assays The Journal of biological chemistry Medium 32115405

Source papers

Stage 0 corpus · 65 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Recruitment and activation of mRNA decay enzymes by two ARE-mediated decay activation domains in the proteins TTP and BRF-1. Genes & development 413 15687258
2007 TTP and BRF proteins nucleate processing body formation to silence mRNAs with AU-rich elements. Genes & development 201 17369404
2002 Functional cloning of BRF1, a regulator of ARE-dependent mRNA turnover. The EMBO journal 183 12198173
2004 Roles of AUF1 isoforms, HuR and BRF1 in ARE-dependent mRNA turnover studied by RNA interference. Nucleic acids research 159 14976220
2011 The roles of TTP and BRF proteins in regulated mRNA decay. Wiley interdisciplinary reviews. RNA 133 21278925
2004 The ARE-dependent mRNA-destabilizing activity of BRF1 is regulated by protein kinase B. The EMBO journal 125 15538381
1994 Conserved functional domains of the RNA polymerase III general transcription factor BRF. Genes & development 114 7995525
2015 BRF1 mutations alter RNA polymerase III-dependent transcription and cause neurodevelopmental anomalies. Genome research 94 25561519
2000 A TRF1:BRF complex directs Drosophila RNA polymerase III transcription. Cell 86 10850489
2006 BRF1 protein turnover and mRNA decay activity are regulated by protein kinase B at the same phosphorylation sites. Molecular and cellular biology 79 17030608
2008 The AU-rich element mRNA decay-promoting activity of BRF1 is regulated by mitogen-activated protein kinase-activated protein kinase 2. RNA (New York, N.Y.) 72 18326031
1996 RNA polymerase III transcription from the human U6 and adenovirus type 2 VAI promoters has different requirements for human BRF, a subunit of human TFIIIB. Molecular and cellular biology 67 8943358
2000 The Brf and TATA-binding protein subunits of the RNA polymerase III transcription factor IIIB mediate position-specific integration of the gypsy-like element, Ty3. The Journal of biological chemistry 64 10882723
1998 Functional and structural organization of Brf, the TFIIB-related component of the RNA polymerase III transcription initiation complex. Molecular and cellular biology 58 9710642
2007 Human Maf1 negatively regulates RNA polymerase III transcription via the TFIIB family members Brf1 and Brf2. International journal of biological sciences 54 17505538
1997 Domains of the Brf component of RNA polymerase III transcription factor IIIB (TFIIIB): functions in assembly of TFIIIB-DNA complexes and recruitment of RNA polymerase to the promoter. Molecular and cellular biology 48 9271407
1998 Polymerase (Pol) III TATA box-binding protein (TBP)-associated factor Brf binds to a surface on TBP also required for activated Pol II transcription. Molecular and cellular biology 45 9488486
1996 Cloning and functional characterization of the gene encoding the TFIIIB90 subunit of RNA polymerase III transcription factor TFIIIB. The Journal of biological chemistry 45 8662956
2006 Novel TRF1/BRF target genes revealed by genome-wide analysis of Drosophila Pol III transcription. The EMBO journal 39 17170711
2017 Role of Brf1 interaction with ERα, and significance of its overexpression, in human breast cancer. Molecular oncology 37 28972307
2016 The significance of Brf1 overexpression in human hepatocellular carcinoma. Oncotarget 33 26701855
2010 Alcohol induces RNA polymerase III-dependent transcription through c-Jun by co-regulating TATA-binding protein (TBP) and Brf1 expression. The Journal of biological chemistry 33 21106530
2017 Association Between Germline Mutations in BRF1, a Subunit of the RNA Polymerase III Transcription Complex, and Hereditary Colorectal Cancer. Gastroenterology 31 28912018
2013 Mapping the protein interaction network for TFIIB-related factor Brf1 in the RNA polymerase III preinitiation complex. Molecular and cellular biology 29 24277937
2005 Reconfiguring the connectivity of a multiprotein complex: fusions of yeast TATA-binding protein with Brf1, and the function of transcription factor IIIB. Proceedings of the National Academy of Sciences of the United States of America 29 16227432
2000 Alternatively spliced hBRF variants function at different RNA polymerase III promoters. The EMBO journal 27 10921893
2016 BRF1 mutations in a family with growth failure, markedly delayed bone age, and central nervous system anomalies. Clinical genetics 26 27748960
2008 Differential expression of the TFIIIB subunits Brf1 and Brf2 in cancer cells. BMC molecular biology 25 18700021
1997 Apolipoprotein B gene regulatory factor-2 (BRF-2) is structurally and immunologically highly related to hepatitis B virus X associated protein-1 (XAP-1). Biochemistry 25 9020796
2014 Brf1 posttranscriptionally regulates pluripotency and differentiation responses downstream of Erk MAP kinase. Proceedings of the National Academy of Sciences of the United States of America 24 24733888
2018 BRF1 ameliorates LPS-induced inflammation through autophagy crosstalking with MAPK/ERK signaling. Genes & diseases 22 30320187
2007 Vaccinia virus-mediated cell cycle alteration involves inactivation of tumour suppressors associated with Brf1 and TBP. Cellular microbiology 21 17877750
2006 Mapping the principal interaction site of the Brf1 and Bdp1 subunits of Saccharomyces cerevisiae TFIIIB. The Journal of biological chemistry 20 16551611
2003 The Brf1 and Bdp1 subunits of transcription factor TFIIIB bind to overlapping sites in the tetratricopeptide repeats of Tfc4. The Journal of biological chemistry 18 12930823
2016 The cAMP pathway regulates mRNA decay through phosphorylation of the RNA-binding protein TIS11b/BRF1. Molecular biology of the cell 16 27708140
2011 A novel function of Tis11b/BRF1 as a regulator of Dll4 mRNA 3'-end processing. Molecular biology of the cell 15 21832157
1995 The human immediate early gene BRF1 maps to chromosome 14q22-q24. Genomics 15 8595910
2015 BRF1, a subunit of RNA polymerase III transcription factor TFIIIB, is essential for cell growth of Trypanosoma brucei. Parasitology 14 26337955
2006 Interactions of Brf1 peptides with the tetratricopeptide repeat-containing subunit of TFIIIC inhibit and promote preinitiation complex assembly. Molecular and cellular biology 14 16880507
2020 The transcription factor Sp1 modulates RNA polymerase III gene transcription by controlling BRF1 and GTF3C2 expression in human cells. The Journal of biological chemistry 13 32115405
2019 Targeting AU-rich element-mediated mRNA decay with a truncated active form of the zinc-finger protein TIS11b/BRF1 impairs major hallmarks of mammary tumorigenesis. Oncogene 13 30914800
2002 A gain-of-function mutation in the second tetratricopeptide repeat of TFIIIC131 relieves autoinhibition of Brf1 binding. Molecular and cellular biology 12 12167707
2019 Brf1 loss and not overexpression disrupts tissues homeostasis in the intestine, liver and pancreas. Cell death and differentiation 10 30858608
2019 Alcohol Intake and Abnormal Expression of Brf1 in Breast Cancer. Oxidative medicine and cellular longevity 10 31781337
2018 RNF12 catalyzes BRF1 ubiquitination and regulates RNA polymerase III-dependent transcription. The Journal of biological chemistry 10 30413534
2001 A role for TAF3B2 in the repression of human RNA polymerase III transcription in nonproliferating cells. The Journal of biological chemistry 10 11283026
2020 Mitogen- and Stress-Activated Protein Kinase 1 Mediates Alcohol-Upregulated Transcription of Brf1 and tRNA Genes to Cause Phenotypic Alteration. Oxidative medicine and cellular longevity 9 32685086
2018 The TFIIE-related Rpc82 subunit of RNA polymerase III interacts with the TFIIB-related transcription factor Brf1 and the polymerase cleft for transcription initiation. Nucleic acids research 9 29177422
2008 Structural characterization of the interaction between TFIIIB components Bdp1 and Brf1. Biochemistry 8 19086269
1999 The product of the primary response gene BRF1 inhibits the interaction between 14-3-3 proteins and cRaf-1 in the yeast trihybrid system. DNA and cell biology 8 10463061
1992 Transcriptional regulation of the apolipoprotein B100 gene: purification and characterization of trans-acting factor BRF-2. Molecular and cellular biology 8 1620125
2021 Participation of TFIIIB Subunit Brf1 in Transcription Regulation in the Human Pathogen Leishmania major. Genes 7 33669344
2020 The significance of Runx2 mediating alcohol-induced Brf1 expression and RNA Pol III gene transcription. Chemico-biological interactions 7 32198086
2020 Expanding the phenotype of cerebellar-facial-dental syndrome: Two siblings with a novel variant in BRF1. American journal of medical genetics. Part A 7 32896090
1998 Identification of a putative BRF homologue in the genome of Caenorhabditis elegans. DNA sequence : the journal of DNA sequencing and mapping 6 9773276
2004 Inhibition of TATA binding protein dimerization by RNA polymerase III transcription initiation factor Brf1. The Journal of biological chemistry 5 15190063
1997 Analysis of a 17.9 kb region from Saccharomyces cerevisiae chromosome VII reveals the presence of eight open reading frames, including BRF1 (TFIIIB70) and GCN5 genes. Yeast (Chichester, England) 5 9133742
2021 Exploring the Role and Mechanism of pAMPKα-Mediated Dysregulation of Brf1 and RNA Pol III Genes. Oxidative medicine and cellular longevity 4 33995823
2021 ROS Signaling-Mediated Novel Biological Targets: Brf1 and RNA Pol III Genes. Oxidative medicine and cellular longevity 3 34646425
2006 The Saccharomyces cerevisiae RNA polymerase III recruitment factor subunits Brf1 and Bdp1 impose a strict sequence preference for the downstream half of the TATA box. Nucleic acids research 3 17028095
2003 Cloning of a putative Bombyx mori TFIIB-related factor (BRF). Archives of insect biochemistry and physiology 2 14518004
2024 Identification of novel variants in BRF1 gene from patient with developmental delay, hearing abnormality, and nervous system anomalies. International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience 1 39005000
2024 BRF1 promotes the odontogenic differentiation of dental pulp stem cells in pulpitis by inducing autophagy. Heliyon 1 39229529
2024 Downregulation of Brf1 Induces Liver Failure and Inhibits Hepatocellular Carcinoma Progression by Promoting Apoptosis. Journal of Cancer 1 39308682
2024 Retracted: ROS Signaling-Mediated Novel Biological Targets: Brf1 and RNA Pol III Genes. Oxidative medicine and cellular longevity 0 38234569

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