| 2008 |
BRD7 is a novel subunit of the PBAF (Polybromo-associated BRG1-associated factor) SWI/SNF chromatin-remodeling complex, distinct from the BAF complex; knockdown of BRD7 (PBAF-specific) and ARID1A (BAF-specific) differentially and sometimes antagonistically regulate SWI/SNF target genes, and SWI/SNF affects recruitment of preinitiation complex components at target promoters. |
Mass spectrometry-based complex purification, shRNA knockdown, gene expression profiling, preinitiation complex recruitment assays |
The Journal of biological chemistry |
High |
18809673
|
| 2010 |
BRD7 physically interacts with p53 and p300, is recruited to p53 target gene promoters, and is required for efficient p53-mediated transcription of a subset of target genes; BRD7 affects histone acetylation and p53 acetylation at these promoters, supporting oncogene-induced senescence. |
Co-immunoprecipitation, ChIP, shRNA knockdown, luciferase reporter assays, senescence assays |
Nature cell biology |
High |
20228809 20660729
|
| 2010 |
BRD7 directly binds BRCA1 (identified by yeast two-hybrid, confirmed by co-immunoprecipitation of endogenous proteins), and is required for BRCA1-mediated transcriptional regulation; BRD7 depletion prevents recruitment of BRCA1 and Oct-1 to the ESR1 promoter, reducing ERα expression, without affecting recruitment of other SWI/SNF subunits (BRG1, BAF155, BAF57) or RNA Pol II. |
Yeast two-hybrid, endogenous co-immunoprecipitation, ChIP, microarray expression profiling, shRNA knockdown |
Cancer research |
High |
20215511
|
| 2006 |
BRD7's bromodomain binds acetylated histone H3 (specifically H3K14ac), co-localizes with acetylated H3 in the nucleus, and this interaction is required for BRD7-mediated transcriptional regulation of E2F3 and inhibition of G1-S cell cycle progression; a bromodomain-deleted BRD7 mutant fails to bind acetylated H3 peptide and loses these functions. |
Co-localization immunofluorescence, histone peptide pull-down, bromodomain deletion mutant analysis, luciferase reporter assay, flow cytometry |
Journal of cellular biochemistry |
High |
16265664
|
| 2007 |
NMR solution structure of the BRD7 bromodomain reveals a typical left-handed four-helix bundle topology; NMR titration experiments show it binds with weak affinity to acetylated lysine peptides from H3 (K9ac, K14ac) and H4 (K8ac, K12ac, K16ac), lacking inherent binding specificity among these marks in vitro. |
NMR spectroscopy (structure determination and titration) |
Biochemical and biophysical research communications |
High |
17498659
|
| 2006 |
BRD7 contains a functional nuclear localization signal (NLS) spanning amino acids 65–96 composed of bipartite nuclear targeting sequences; deletion of the NLS shifts BRD7 localization from nucleus to cytoplasm and abolishes its ability to regulate cyclin D1, E2F3 expression, and G1-S cell cycle progression. |
GFP fusion constructs, deletion mutagenesis, fluorescence microscopy, western blot, flow cytometry |
Journal of cellular biochemistry |
Medium |
16475162
|
| 2014 |
BRD7 interacts with the inter-SH2 (iSH2) domain of p85α (PI3K regulatory subunit) via a conserved C-terminal region, facilitates nuclear translocation of p85α, depletes cytosolic p85/p110 complexes, and thereby reduces p110 protein stability and PI3K/Akt pathway signaling; BRD7 and p110 compete for binding to p85. |
Co-immunoprecipitation, domain mapping, RNAi knockdown, Akt phosphorylation assays, subcellular fractionation |
Molecular cell |
High |
24657164
|
| 2014 |
BRD7 interacts with regulatory subunits of PI3K (p85α and p85β) and promotes nuclear translocation of both p85 isoforms and the spliced form of XBP1 (XBP1s); BRD7 deficiency blocks nuclear translocation of XBP1s, impairing the unfolded protein response (UPR); restoring hepatic BRD7 in obese mice improves XBP1s nuclear translocation and glucose homeostasis. |
Co-immunoprecipitation, subcellular fractionation, in vivo mouse models (adenoviral BRD7 restoration), glucose tolerance tests |
Cell metabolism |
High |
24836559
|
| 2003 |
BRD7 (Celtix-1/BP75) forms a complex with the heterogeneous nuclear ribonucleoprotein E1B-AP5 both in vivo and in vitro; disruption of this complex increases E1B-AP5 transcriptional repression activity and converts E1B-AP5 from an activator to a strong repressor of hormone-dependent promoters; BRD7 bromodomain binds histones H2A, H2B, H3, and H4, and a triple complex of E1B-AP5, BRD7, and histones was demonstrated. |
Yeast two-hybrid, in vivo and in vitro co-immunoprecipitation, GST pull-down, luciferase reporter assays, deletion mutagenesis |
The Biochemical journal |
High |
12489984
|
| 2000 |
BRD7 (Celtix-1) interacts with IRF-2 via the C-terminus of IRF-2, as established by yeast two-hybrid and GST pull-down; a subset of BRD7/Celtix-1 co-localizes with hyperacetylated histones H3/H4 and the hyperphosphorylated (active) form of RNA Pol II in the nucleus. |
Yeast two-hybrid, GST pull-down, immunofluorescence co-localization |
Journal of cellular physiology |
Medium |
11025449
|
| 1999 |
BP75 (BRD7) was identified through interaction with the first PDZ domain of protein tyrosine phosphatase PTP-BL in a yeast two-hybrid screen; both BP75 and a PTP-BL PDZ domain construct localize primarily to the nucleus. |
Yeast two-hybrid, subcellular localization by immunofluorescence |
FEBS letters |
Low |
10526152
|
| 2003 |
BP75 (BRD7) directly interacts with Dvl-1 (Dishevelled-1), enhances TCF-dependent gene expression induced by Dvl-1, facilitates dephosphorylation of GSK-3β at Tyr216 thereby inhibiting its kinase activity, and synergizes with Dvl-1 to promote nuclear translocation of β-catenin. |
Yeast two-hybrid, co-immunoprecipitation in mammalian cells, TCF luciferase reporter assay, GSK-3β kinase assay, β-catenin localization |
Cancer research |
Medium |
12941796
|
| 2009 |
BRD7 interacts with TRIM24/TIF1α and represses TRIM24-enhanced androgen receptor (AR) transactivation activity, as measured by luciferase reporter assay in prostate cancer cells. |
Co-immunoprecipitation, luciferase reporter assay |
Biochimica et biophysica acta |
Low |
19909775
|
| 2004 |
Ectopic BRD7 expression in NPC cells inhibits G1-S progression and transcriptionally regulates molecules in the Ras/MEK/ERK and Rb/E2F pathways; BRD7 negatively regulates E2F3 promoter activity. |
Tet-on inducible expression, cell cycle cDNA array, luciferase reporter assay, flow cytometry |
Journal of cellular physiology |
Medium |
15137061
|
| 2019 |
PARP-1 binds to BRD7 and poly(ADP-ribosyl)ates it; this modification enhances BRD7 ubiquitination and degradation through the PAR-binding E3 ubiquitin ligase RNF146, leading to BRD7 degradation in response to DNA damage-inducing chemotherapy. |
Co-immunoprecipitation, PAR assay (PARylation), ubiquitination assay, RNF146 knockdown, western blot for protein stability |
EMBO reports |
High |
30940648
|
| 2014 |
BRD7 forms a complex with the APC/C (anaphase-promoting complex/cyclosome) and is degraded by APC/C(Cdh1) and APC/C(Cdc20) during the cell cycle; a BRD7 mutant resistant to APC/C-mediated degradation more efficiently suppresses osteosarcoma proliferation and tumor growth. |
Co-immunoprecipitation, protein stability assay, APC/C inhibitor (proTAME), APC/C degradation-resistant mutant, in vitro and in vivo tumor growth assays |
Oncotarget |
Medium |
24840027
|
| 2020 |
BRD7 expression is increased by inhibition of the ubiquitin-proteasome pathway upon ferroptosis induction; elevated BRD7 promotes p53 mitochondrial translocation via direct binding to the p53 N-terminal transactivation domain (TAD); site-directed mutation of p53 serine 392 blocks BRD7-p53 binding and prevents p53 mitochondrial translocation and ferroptosis; mitochondrial p53 then interacts with SLC25A28 to enhance its activity, leading to iron accumulation and ferroptosis. |
CRISPR/Cas9 knockout, BRD7 overexpression plasmid, co-immunoprecipitation, site-directed mutagenesis, subcellular fractionation, SLC25A28 knockdown |
Redox biology |
High |
32863216
|
| 2020 |
BRD7 is recruited to DNA double-strand break (DSB) sites via ATM-mediated phosphorylation; at DSBs, BRD7 joins PRC2 and NuRD complexes and recruits E3 ubiquitin ligase RNF168, leading to transcriptional repression at active transcription sites flanking DSBs and facilitating DNA repair. |
Co-immunoprecipitation, ChIP, immunofluorescence, ATM inhibitor treatment, phosphorylation site mapping, RNF168 recruitment assay, DNA repair assays |
Advanced science |
High |
33101843
|
| 2020 |
BRD7 interacts with YB1 via its N-terminus binding to the C-terminus of YB1; BRD7 decreases YB1 expression by negatively regulating YB1 phosphorylation at Ser102, promoting its proteasomal degradation, thereby suppressing YB1-induced epithelial-mesenchymal transition (EMT), invasion, and metastasis in breast cancer. |
Co-immunoprecipitation with mass spectrometry, deletion mutant mapping, phosphorylation assay, ubiquitination/proteasome assay, in vitro migration/invasion assays, xenograft and metastatic mouse models |
Journal of experimental & clinical cancer research |
High |
32028981
|
| 2008 |
BRD7 interacts with BRD2 (co-immunoprecipitation confirmed in mammalian cells); the region from amino acids 430–798 of BRD2 is critical for this interaction; BRD2 localizes in the nucleus in diffuse and dotted patterns. |
Co-immunoprecipitation, GFP fluorescence, deletion mutant analysis |
Molecular and cellular biochemistry |
Low |
16786191
|
| 2008 |
The centrosome-associated protein Ceap-16/BLOS2 directly interacts with BRD7 via BRD7's C-terminus and Ceap-16's central region; this interaction translocates Ceap-16 from cytoplasm to nucleus, where it selectively inhibits BRD7's transcriptional suppression of target genes (E2F3, cyclin A); a triple complex of Ceap-16, BRD7, and histones H3/H4 was demonstrated. |
Co-immunoprecipitation (in vitro and in vivo), domain mapping, reporter assays, localization studies |
Cellular signalling |
Medium |
18329849
|
| 2016 |
BRD7 knockout mice display an anti-inflammatory phenotype deficiency: BRD7-deficient MEF cells show increased NF-κB (p65) cytoplasm-to-nucleus translocation and elevated inflammatory cytokine expression (IL-6, TNF-α, CXCL-1, iNOS) after LPS stimulation; in vivo, BRD7 KO mice show increased susceptibility to DSS-induced colitis with higher NF-κB nuclear translocation, indicating BRD7 inhibits NF-κB activation during early acute inflammation. |
BRD7 knockout mouse model, MEF cells, LPS stimulation, NF-κB reporter assay, subcellular fractionation, DSS-induced colitis model |
Cellular & molecular immunology |
Medium |
27374794
|
| 2016 |
Homozygous BRD7 knockout results in complete male infertility with spermatogenesis arrest at step 13, deformed acrosomal formation, degenerative elongating spermatids, increased apoptosis (TUNEL, annexin V, p53), and elevated DNA damage marker γH2AX; BRD7 is highly expressed in testis and localized to germ cells from pachytene to round spermatid stage. |
BRD7 knockout mouse model, histology, TUNEL assay, western blot for apoptosis/DNA damage markers, immunohistochemistry |
Scientific reports |
Medium |
26878912
|
| 2015 |
BRD7 knockout impairs cognitive behavior (but not emotional behavior) and reduces synaptic plasticity-related protein expression, neuronal spine density, and dendritic branching specifically in the medial prefrontal cortex (not hippocampus). |
BRD7 knockout mouse model, behavioral battery tests, western blot for synaptic proteins, neuronal morphology analysis |
Behavioural brain research |
Medium |
25721744
|
| 2016 |
BRD7 deficiency leads to embryonic lethality in homozygous knockout mice at mid-gestation (prior to E16.5), establishing an essential developmental role; heterozygous knockdown causes mild changes in glucose metabolism. |
Homozygous and heterozygous BRD7 knockout mouse models, embryo developmental staging, glucose metabolism assays |
Journal of cellular and molecular medicine |
Medium |
27444544
|
| 2017 |
BRD7 increases phosphorylation of GSK3β at Ser9 in response to insulin, with this effect occurring even in the absence of AKT activity; BRD7 also mediates phosphorylation of S6K and downstream 4E-BP1; liver-specific BRD7 knockout mice show impaired mTORC1 activity on its downstream targets. |
BRD7 overexpression, AKT inhibitor, liver-specific BRD7 KO mice, phosphorylation assays (western blot), in vitro and in vivo models |
Cellular and molecular life sciences |
Medium |
29127434
|
| 2018 |
BRD7 directly interacts with HIF1α and facilitates its degradation via the ubiquitin-proteasome pathway; this reduces LDHA expression and aerobic glycolysis (Warburg effect) in breast cancer cells; bromodomain of BRD7 is required for this activity. |
Co-immunoprecipitation, ubiquitination assay, bromodomain deletion mutant, LDHA rescue experiment, glycolysis assays, in vivo tumor models |
Cell death & disease |
Medium |
29725006
|
| 2024 |
TRIM28 acts as an E3 ubiquitin ligase for BRD7; the Coiled-Coil region of TRIM28 binds the N-terminal region of BRD7, mediating K48-linked ubiquitination of BRD7 at K21, leading to proteasomal degradation of BRD7 and promoting breast cancer progression. |
Co-immunoprecipitation with mass spectrometry, domain mapping, ubiquitination assay (K48 linkage), site-directed mutagenesis (K21), protein stability assay, in vitro and in vivo cancer models |
Cellular oncology |
High |
39222175
|
| 2025 |
TRIM25 acts as an E3 ubiquitin ligase for BRD7; the PRYSPRY region of TRIM25 binds the N-terminal region of BRD7, increasing K48-linked ubiquitination at K119 and promoting BRD7 proteasomal degradation; this leads to activation of YB1/Bcl-2 signaling, promoting breast cancer malignant progression and paclitaxel resistance. |
Co-immunoprecipitation, ubiquitination assay (K48-linked, K119 site), domain mapping, protein stability assay, rescue experiment with BRD7 restoration, in vitro and in vivo models |
Cell death & disease |
Medium |
41315221
|
| 2022 |
BRD7 stabilizes p53 protein by inhibiting AKT-dependent phosphorylation of MDM2 (via the BRD7 bromodomain), thereby reducing phospho-MDM2 binding to p53 and decreasing p53 ubiquitination; this mechanism requires the BRD7 bromodomain. |
Co-immunoprecipitation, phosphorylation assay, ubiquitination assay, bromodomain deletion mutant, AKT inhibition, p53 knockdown rescue, in vivo xenograft |
Journal of Cancer |
Medium |
35371302
|
| 2021 |
In colorectal cancer, BRD7 interacts with c-Myc and stabilizes c-Myc protein by inhibiting its ubiquitin-proteasome-dependent degradation; restoration of c-Myc in BRD7-silenced CRC cells rescues cell proliferation and tumor growth. |
Co-immunoprecipitation, ubiquitination assay, c-Myc rescue experiment, in vitro and in vivo tumor models, AOM/DSS mouse model |
Frontiers in cell and developmental biology |
Medium |
34109174
|
| 2023 |
BRD7 negatively regulates BIRC2 expression by targeting and inhibiting the activity of the B7BS enhancer region of BIRC2; restoration of BIRC2 rescues the tumor suppressive effects of BRD7 on NPC cell proliferation, migration, invasion, and xenograft tumor growth. |
ChIP, luciferase enhancer reporter assay, BIRC2 rescue experiment, in vitro and in vivo tumor models |
Cell death & disease |
Medium |
36788209
|
| 2024 |
BRD7 bridges BRG1 and PBRM1 to the core module of the PBAF complex during CD8+ T cell activation, facilitating PBAF assembly over BAF; the resulting PBAF complex increases chromatin accessibility at the Tbx21 locus and upregulates T-bet expression, driving maturation of short-lived effector CD8+ T cells. |
BRD7 conditional knockout in CD8+ T cells, co-immunoprecipitation, ATAC-seq (chromatin accessibility), flow cytometry, viral infection models (influenza, LCMV) |
JCI insight |
High |
38954484
|
| 2023 |
BRD7 competitively inhibits binding of the deubiquitinase USP5 to METTL3, reducing METTL3 protein stability via the ubiquitin-proteasome pathway; this suppresses BRCA1- and RAD51-mediated homologous recombination repair, increasing radiosensitivity of NPC cells. |
Co-immunoprecipitation, competitive binding assay (BRD7 vs USP5 for METTL3), ubiquitination assay, DNA damage (DSB) assays, homologous recombination repair assays |
International journal of biological sciences |
Medium |
39664566
|
| 2024 |
BRD7 directly binds EZH2 and recruits DNMT3a to the Clusterin promoter, modulating Clusterin promoter hypermethylation; reduced Clusterin expression suppresses AMPK signaling to facilitate ferroptosis in diabetic testicular damage. |
Co-immunoprecipitation (BRD7-EZH2, BRD7-DNMT3a), methylation-specific PCR, ChIP assay, BRD7 knockdown, Clusterin rescue experiment |
Molecular medicine |
Medium |
38992588
|
| 2023 |
BRD7 silencing stabilizes CHK1 (but not CHK2) by increasing USP1 levels and promoting the CHK1-USP1 interaction, enhancing CHK1 deubiquitination; USP1 knockdown abrogates BRD7 silencing-induced CHK1 induction, establishing BRD7 as a negative regulator of CHK1 through the USP1 deubiquitinase axis. |
BRD7 siRNA, CHK1/CHK2 western blot, co-immunoprecipitation (CHK1-USP1), ubiquitination assay, USP1 knockdown rescue, apoptosis assay |
Cell death discovery |
Medium |
37626049
|
| 2011 |
miR-200c directly inhibits BRD7 expression; BRD7 loss induced by miR-200c leads to β-catenin nuclear translocation and increased expression of cyclin D1 and c-Myc in endometrial carcinoma cells. |
miRNA transfection, mRNA microarray, western blot, β-catenin localization assay |
Gynecologic oncology |
Low |
22015043
|
| 2016 |
BRD7 acts as a transcription factor to up-regulate the expression of miR-3148 at the transcriptional level; miR-3148 then targets the 3'UTR of Wnt3a mRNA to suppress Wnt3a/β-catenin signaling in cervical cancer cells. |
BRD7 overexpression, luciferase reporter assay for miR-3148 promoter activity, 3'UTR luciferase assay for Wnt3a targeting, western blot |
Reproductive sciences |
Low |
32046432
|
| 2023 |
BRD7 interacts with InsR (insulin receptor) as shown by co-immunoprecipitation; BRD7 improves glucose homeostasis in liver-specific IRS1/2 double knockout mice, demonstrating that BRD7's effect on insulin signaling operates through an IRS-independent alternative pathway downstream of InsR. |
Co-immunoprecipitation (BRD7-InsR), liver-specific InsR KO and IRS1/2 KO mouse models, glucose tolerance and insulin signaling assays |
The Journal of endocrinology |
Medium |
37578842
|
| 2025 |
Brd7 loss in breast cancer metastatic dormancy models induces metastatic reawakening; Brd7-deficient cells downregulate MHC-1 expression and promote a pro-metastatic cytokine profile, increasing pro-tumorigenic neutrophils, CD8+ exhausted T cells, and CD4+ stress-response T cells in the lung microenvironment; neutrophil depletion, NET inhibition, or immune checkpoint therapy abrogates this metastatic outgrowth. |
In vivo PBAF subunit screen, flow cytometry, single-cell RNA-seq, epigenomic profiling, neutrophil depletion, NET inhibition, immune checkpoint therapy |
Nature communications |
High |
39910049
|