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Bromodomain-containing protein 2 (BRD2) interactome in ES cells

ABSTRACT: Identification of Bromodomain-containing protein 2 (BRD2) interaction partners using liquid-chromatography based mass spectrometry in murine embryonic stem cells (ESC), using BRD2 endogenously tagged with a mAID-V5 tag.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture, Embryonic Stem Cell

SUBMITTER: Alejandro Gomez-Auli

LAB HEAD: Gerhard Mittler

PROVIDER: PXD072982 | Pride | 2026-04-22

REPOSITORIES: Pride

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			Action	DRS
	00002632___A_AID_1_inj01.raw	Raw
	00002632___A_AID_1_inj02.raw	Raw
	00002632___A_AID_1_inj03.raw	Raw
	00002632___A_AID_1_test.raw	Raw
	00002633___B_AID_2_inj01.raw	Raw

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1 - 5 of 22

Publications

Histone acetylation-dependent clustering of BRD2 instructs transcription dynamics.

Erdogdu Niyazi Umut NU Guhathakurta Sukanya S Oellers Ronald R Shvedunova Maria M Morin Jose A JA Patrick Eric M EM Seyfferth Janine J Deboutte Ward W Gomez-Auli Alejandro A Mittler Gerhard G Cissé Ibrahim I II Akhtar Asifa A

Nature genetics 20260409 4

Bromodomain (BD) and extra-terminal domain (BET) proteins are key regulators of RNA polymerase II (Pol II)-mediated transcription and their BDs represent promising drug targets. Yet, the interplay between histone acetylation and the chromatin dynamics of individual BET proteins with respect to transcriptional regulation is not fully understood. Here in mouse embryonic stem cells, we uncover an essential role of BRD2 in maintaining Pol II recruitment at promoters through its interaction with TFII ...[more]

PMID: 41957181

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Haploinsufficiency in bromodomain containing 2 (Brd2) gene remodels synaptic transmission in male mouse striatum

Project description:Our previous work confirmed that Brd2+/- mouse presents the sex specific characteristics of juvenile myoclonic epilepsy, a subsyndrome of idiopathic generalized epilepsy. Here, we investigated the role of Brd2 gene in modulating the genomic fabrics responsible for the glutamatergic, GABAergic, dopaminergic, cholinergic and serotonergic transmission in the front cortex striata of male mice. Agilent two-color gene expression arrays and the genomic fabric paradigm were used to determine whether the expression and networking of genes involved in the synaptic transmission differ between Brd2+/- and wildtype mice. We found relatively few regulated genes in Brd2+/-mice with respect to their wildtype counterparts. However, most of the regulated genes were directly related to control of anxiety and seizures, justifying the role of Brd2 upstream control of these traits. Agilent mouse two-color gene expression arrays to profile striata of the prefrontal cortices of wildtype (W) and Brd2+/- (H) mouse male (M) adult C57Bl/6j mice. Differently labeled biological replicates were cohybridized with each array. Results of similarly labeled different conditions were compared then averaged for the two fluorescent labels. For instance: MW1 & MW3 were compared with MH1 & MH3, MW2 & MW4 were compared with MH2 & + MH4, and the results of the comparisons averaged. This design uses 100% of the resources, has a better normlaiztion and allows all possible comparisons among the conditions.

2015-09-01 | E-GEOD-72562 | biostudies-arrayexpress

Haploinsufficiency in bromodomain containing 2 (Brd2) gene remodels synaptic transmission in male mouse striatum

2015-09-01 | GSE72562 | GEO

Affinity-purification MS of Drosophila melanogaster’s dSetDB1

Project description:Evaluation of binding partners of wild-type endogenously tagged flag-HA-dSetDB1 versus catalytic dead endogenously tagged flag-HA-250 dSetDB1 in Drosophila melanogaster early embryos

2024-06-07 | PXD045480 | Pride

Haploinsufficiency in bromodomain containing 2 (Brd2) gene remodels synaptic transmission in female mouse striatum in a sex-specific manner

Project description:Our previous work showed that Brd2+/- mouse models the sex specific characteristics of juvenile myoclonic epilepsy, a subsyndrome of idiopathic generalized epilepsy. Here, we investigated a role of Brd2 gene in modulating the genomic fabrics responsible for the glutamatergic, GABAergic, dopaminergic, cholinergic and serotonergic transmission in the striatum of female mice. Agilent two-color gene expression arrays and the genomic fabric paradigm were used to determine whether the expression and networking of genes involved in the synaptic transmission differ between Brd2+/- and wildtype mice and whether these differences are sex-specific. As in Brd+/- male mice we found relatively few regulated genes in Brd2+/-female mice with respect to their wildtype counterparts. However, most of the regulated genes were directly related to control of anxiety and seizures, justifying the role of Brd2 upstream control of these traits. Remarkably, the sets of regulated genes in the two sexes did not overlap, supporting the conclusion of sex-specific control of traits by Brd2. Agilent mouse two-color gene expression arrays to profile striata of the prefrontal cortices of wildtype (W) and Brd2+/- (H) mouse female (F) adult C57Bl/6j mice. Differently labeled biological replicates were cohybridized with each array. Results of similarly labeled different conditions were compared then averaged for the two fluorescent labels. For instance: FW1 & FW3 were compared with FH1 & FH3, FW2 & FW4 were compared with FH2 & + FH4, and the results of the comparisons averaged. This design uses 100% of the resources, has a better normlaiztion and allows all possible comparisons among the conditions.

2015-09-01 | E-GEOD-72563 | biostudies-arrayexpress

Affinity Purification experiments for 24 human Bromodomain proteins involved in DNA repair and genome integrity (part 1 of 2).

Project description:Bromodomain proteins (BRD) are key chromatin regulators of genome function and stability, as well as therapeutic targets in cancer. In our associated publication (doi:10.1101/gad.331231.119) we systematically delineate the contribution of human BRD proteins for genome stability and DNA double-strand break (DSB) repair using cell-based assays and proteomic interaction network analysis. These AP-MS experiments were performed in order to construct a protein interaction network for the 24 BRDs we identified as promoters of DNA repair and/or genome integrity: BAZ1B, BRD1, BRD2, BRD3, BRD4, BRD8, BRD9, BRPF3, BRWD3, CECR2, EP300, GCN5/KAT2A, PCAF/KAT2B, PHIP, SMARCA2, SP100, SP110, SP140, TAF1, TRIM24, TRIM28, TRIM33, TRIM66, ZMYND8. In combination with cell based assays, we identified a BRD-reader function of PCAF that bound TIP60-mediated histone acetylations at DSBs to recruit a DUB complex to deubiquitylate histone H2BK120, to allow direct acetylation by PCAF and repair of DSBs by homologous recombination. We also discovered the bromo-and-extra-terminal (BET) BRD proteins, BRD2 and BRD4, as negative regulators of transcription-associated RNA-DNA hybrid (R-Loop) as inhibition of BRD2 or BRD4 increased R-loop formation, which generated DSBs. These breaks were reliant on Topoisomerase II and BRD2 directly bound and activated Topoisomerase I, a known restrainer of R-loops. Thus, comprehensive interactome and functional profiling of BRD proteins revealed new homologous recombination and genome stability pathways, providing a strategy to understand genome maintenance by BRD proteins and the effects of their pharmacological inhibition. This accession provides AP-MS experiment files for the following subset of 18 BRDs: BAZ1B, BRD1, BRD2, BRD3, BRD4, BRD8, BRPF3, BRWD3, CECR2, PHIP, SMARCA2, SP100, SP110, TAF1, TRIM24, TRIM33, TRIM66, ZMYND8, as well as their associated controls (Input, Mock, and SBP-tagged NLS).

2019-12-12 | PXD016700 | Pride

BRD2 Bromodomain-Mediated Regulation of Cell State Plasticity Modulates Therapy Response in Glioblastoma

Project description:Background: Glioblastoma (GBM) displays remarkable cell state plasticity, a major contributor to therapeutic resistance and tumor progression. While epigenetic mechanisms play a central role in driving this plasticity, the key regulators remain poorly understood, and developing effective therapeutic strategies targeting them has been challenging. Methods: We investigated the role of BRD2, a key regulator of NF-κB mediated mesenchymal (MES) transition, using GBM patient-derived xenograft (PDX) cell lines, CRISPR-mediated knock-in/knockout approaches, RNA-seq, and in vitro and in vivo modeling. BET inhibitors were employed to target MES gene expression and sensitize GBM to radiation therapy. Results: We found that PTEN loss induces RelA chromatin localization and acetylation-mediated recruitment of BRD2 to the MES gene promoters. BRD2 binding is essential for maintaining MES gene expression and phenotype. Genetic ablation or loss-of-function mutation of BRD2 bromodomains reverses MES transition, enhances radiation sensitivity, and improves survival in orthotopic xenograft models. Additionally, treatment with a brain-penetrant BD2-selective inhibitor suppresses the MES phenotype and increases radiation sensitivity of GBM stem cells in vitro. Conclusion: Our study identifies BRD2 as a key mediator of MES transition in GBM, with its bromodomains playing a crucial role in driving cell state plasticity. Targeting BRD2 with BD2-selective inhibitors offers a promising therapeutic strategy to overcome radiation resistance and improve outcomes for GBM patients.

2025-11-17 | GSE304029 | GEO

Haploinsufficiency in bromodomain containing 2 (Brd2) gene remodels synaptic transmission in female mouse striatum in a sex-specific manner

2015-09-01 | GSE72563 | GEO

Affinity Purification experiments for 24 human Bromodomain proteins involved in DNA repair and genome integrity (part 2 of 2)

Project description:Bromodomain proteins (BRD) are key chromatin regulators of genome function and stability, as well as therapeutic targets in cancer. In our associated publication (doi:10.1101/gad.331231.119) we systematically delineate the contribution of human BRD proteins for genome stability and DNA double-strand break (DSB) repair using cell-based assays and proteomic interaction network analysis. These AP-MS experiments were performed in order to construct a protein interaction network for the 24 BRDs we identified as promoters of DNA repair and/or genome integrity: BAZ1B, BRD1, BRD2, BRD3, BRD4, BRD8, BRD9, BRPF3, BRWD3, CECR2, EP300, GCN5/KAT2A, PCAF/KAT2B, PHIP, SMARCA2, SP100, SP110, SP140, TAF1, TRIM24, TRIM28, TRIM33, TRIM66, ZMYND8. In combination with cell based assays, we identified a BRD-reader function of PCAF that bound TIP60-mediated histone acetylations at DSBs to recruit a DUB complex to deubiquitylate histone H2BK120, to allow direct acetylation by PCAF and repair of DSBs by homologous recombination. We also discovered the bromo-and-extra-terminal (BET) BRD proteins, BRD2 and BRD4, as negative regulators of transcription-associated RNA-DNA hybrid (R-Loop) as inhibition of BRD2 or BRD4 increased R-loop formation, which generated DSBs. These breaks were reliant on Topoisomerase II and BRD2 directly bound and activated Topoisomerase I, a known restrainer of R-loops. Thus, comprehensive interactome and functional profiling of BRD proteins revealed new homologous recombination and genome stability pathways, providing a strategy to understand genome maintenance by BRD proteins and the effects of their pharmacological inhibition. This accession provides AP-MS experiment files for the following subset of 6 BRDs: BRD9, EP300, GCN5/KAT2A, PCAF/KAT2B, SP140, TRIM28, as well as their associated controls (Input, Mock, and SBP-tagged NLS).

2019-12-12 | PXD016673 | Pride

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Transcriptional regulation of the innate immune reponse by the MITF/TFE3 family

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2016-02-01 | E-GEOD-75822 | biostudies-arrayexpress

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