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Expression data from murine BRD2-mediated lymphomas

ABSTRACT: The dual bromodomain protein Brd2 is closely related to the basal transcription factor TAFII250, which is essential for cyclin A transactivation and mammalian cell cycle progression. In transgenic mice, constitutive lymphoid expression of Brd2 causes a malignancy most similar to human diffuse large B cell lymphoma. We compare the genome-wide transcriptional expression profiles of these lymphomas with those of proliferating and resting normal B cells. Transgenic tumors reproducibly show differential expression of a large number of genes important for cell cycle control and lymphocyte biology; expression patterns are either tumor-specific or proliferation-specific. Several of their human orthologs have been implicated in human lymphomagenesis. Others correlate with human disease survival time. BRD2 is underexpressed in some subtypes of human lymphoma and these subtypes display a number of similarities to the BRD2-mediated murine tumors. We illustrate with a high degree of detail that cancer is more than rampant cellular proliferation, but involves the additional transcriptional mobilization of many genes, some of them poorly characterized, which show a tumor-specific pattern of gene expression. Keywords: disease state analysis

ORGANISM(S): Mus musculus

PROVIDER: GSE6136 | GEO | 2006/10/28

SECONDARY ACCESSION(S): PRJNA97711

REPOSITORIES: GEO

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Transcription profiling of mouse BRD2-mediated lymphomas

Project description:The dual bromodomain protein Brd2 is closely related to the basal transcription factor TAFII250, which is essential for cyclin A transactivation and mammalian cell cycle progression. In transgenic mice, constitutive lymphoid expression of Brd2 causes a malignancy most similar to human diffuse large B cell lymphoma. We compare the genome-wide transcriptional expression profiles of these lymphomas with those of proliferating and resting normal B cells. Transgenic tumors reproducibly show differential expression of a large number of genes important for cell cycle control and lymphocyte biology; expression patterns are either tumor-specific or proliferation-specific. Several of their human orthologs have been implicated in human lymphomagenesis. Others correlate with human disease survival time. BRD2 is underexpressed in some subtypes of human lymphoma and these subtypes display a number of similarities to the BRD2-mediated murine tumors. We illustrate with a high degree of detail that cancer is more than rampant cellular proliferation, but involves the additional transcriptional mobilization of many genes, some of them poorly characterized, which show a tumor-specific pattern of gene expression. Experiment Overall Design: 26 samples are included in this series. Sporadic murine E-mu-BRD2 mediated lymphomas are divided into three classes by disease severity and compared to either resting or mitogen-activated B Cells. The resting and activated B Cells are either wildtype or E-mu-BRD2 transgenic. All samples are on the FVB wildtype background.

2008-06-14 | E-GEOD-6136 | biostudies-arrayexpress

Brd2 regulates gene expression and alternative splicing.

Project description:We analyzed a role of Brd2 protein in transcription and alternative splicing. 289 genes change alternative splicing after Brd2 knockdown and 1459 genes alter gene expression compared to cells treated with negative control siRNA. 6 samples (3 independent samples of cells treated with Brd2 siRNA, 3 samples of cells treated with negative control siRNA)

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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

The BET protein BRD2 cooperates with CTCF to enforce a transcriptional boundary

Project description:Role of the bromodomain and extraterminal motif (BET) protein BRD2 in CTCF chromatin occupancy, tested by CRISPR/Cas9-mediated depletion of BRD2 in GATA1-null erythroblasts expressing an inducible GATA1-ER fusion (G1E-ER4). Pharmacologic inhibitors of the BET (bromodomain and extraterminal motif) family of proteins are being explored for the treatment of various diseases, including cancer, yet the individual functions of BET proteins remain unclear. Here we find that BRD2 co-localizes with the architectural/insulator protein CCCTC-binding factor (CTCF) genome-wide. CTCF recruits BRD2 to co-bound sites, whereas BRD2 is dispensable for CTCF occupancy. Genome editing at a CTCF/BRD2 co-occupied site reveals a functional boundary element that upon perturbation results in transcriptional misregulation. Single-molecule RNA FISH reveals that either site-specific CTCF loss or BRD2 depletion increases the correlation in expression of two genes flanking the boundary. Together these findings indicate that BRD2 supports chromatin boundary activity in a CTCF-dependent manner and suggest that pharmacologic BET inhibitors influence gene expression in part by perturbing chromatin domain boundary function.

2017-03-31 | GSE80527 | GEO

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

Brd2 regulates gene expression and alternative splicing.

2013-12-03 | GSE39937 | GEO

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

2015-09-01 | GSE72562 | 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

BRD2 CUT & RUN in Calu-3 cells

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2021-09-02 | GSE182993 | GEO

Bromodomain and extra-terminal (BET) inhibitors regulate NK cell biology by inhibiting BRD2 mediated NK cytolytic activity and BRD2/BRD4 mediated inflammatory function

Project description:Natural killer cells are innate lymphocytes that play a pivotal role in the immune surveillance and elimination of transformed or virally infected cells. Using a combined chemico-genetic approach, we have identified that BET bromodomains BRD2 and BRD4 are central regulators of NK cell responses. We show that both BRD2 and BRD4 play a key regulatory function in controlling NK cell specific inflammatory responses. However, knockdown of BRD2 but not BRD4 impairs NK cell cytolytic response, highlighting a redundant role for BRD4 in regulating NK cell killing. We further show that the prototypic monovalent BET inhibitor impairs in vitro NK cell mediated killing of cancer target cells, while the bivalent BET bromodomain AZD5153 does not. We ascribe these differences to the preferential affinity of JQ1(+) to BRD2, while AZD5153 has a higher affinity for BRD4. Our work suggests that inhibiting BET bromodomains may be an effective therapeutic strategy for controlling inflammatory function. Given that BRD2 but not BRD4 inhibition can impair NK cell mediated killing, our findings also have clinical significance in light of the ongoing clinical application of BET bromodomains in oncology.

2021-03-16 | GSE156423 | GEO

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