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Links from GEO DataSets

Items: 20

1.

BET Bromodomain inhibition promotes neurogenesis while inhibiting gliogenesis in neural progenitor cells

(Submitter supplied) Neural stem cells (NSCs) and progenitor cells (NPCs) are increasingly appreciated to hold great promise for regenerative medicine to treat CNS injuries and neurodegenerative diseases. However, evidence for effective stimulation of neuronal production from endogenous or transplanted NPCs for cell replacement with small molecules remains limited. To identify novel chemical entities/targets for neurogenesis, we had established a NPC phenotypic screen assay and validated it using known small-molecule neurogenesis inducers. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
24 Samples
Download data: TXT, XLSX
Series
Accession:
GSE77988
ID:
200077988
2.

Targeting the EWS/ETS transcriptional program by BET bromodomain inhibition in Ewing sarcoma

(Submitter supplied) Ewing sarcomas (ES) are highly malignant, osteolytic bone or soft tissue tumors, which are characterized by early metastasis into lung and bone. Genetically, ES are defined by balanced chromosomal EWS/ETS translocations, which give rise to chimeric proteins (EWS-ETS) that generate an oncogenic transcriptional program associated with altered epigenetic marks throughout the genome. By use of an inhibitor (JQ1) blocking BET bromodomain binding proteins (BRDs) we strikingly observed a strong down-regulation of the predominant EWS-ETS protein EWS/FLI1 in a dose dependent manner. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL6244
4 Samples
Download data: CEL
Series
Accession:
GSE72673
ID:
200072673
3.

JQ1 modulates inflammatory related-genes in human renal tubular epithelial cells

(Submitter supplied) Selective bromodomains inhibitors block the interaction between diverse bromodomains and extraterminal domains (BET) proteins and acetylated proteins. These inhibitors have shown beneficial effects in cancers malignancies and experimental inflammation in mouse models, but data on renal diseases are scarce. We have investigated the effect of the BET proteins inhibitor JQ1 in a mice model of unilateral ureteral obstruction. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL10558
3 Samples
Download data: TXT
Series
Accession:
GSE71602
ID:
200071602
4.

SPOP mutation confers intrinsic BET inhibitor resistance in prostate cancer (BRDs_OE_RNA-seq)

(Submitter supplied) Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising therapeutics of cancers including prostate cancer. The E3 ubiquitin ligase adaptor protein speckle-type POZ protein (SPOP) is implicated in human prostate cancers due to its frequent mutation. Here we demonstrate that SPOP binds to the BET proteins BRD2, BRD3 and BRD4. Wild-type SPOP, but not prostate cancer-associated mutants, promotes polyubiquitination and proteasome degradation of BET proteins by recognizing a common degron motif. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: TXT
5.

SPOP mutation confers intrinsic BET inhibitor resistance in prostate cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
26 Samples
Download data: BIGWIG, BW, TXT
Series
Accession:
GSE88872
ID:
200088872
6.

SPOP mutation confers intrinsic BET inhibitor resistance in prostate cancer (ChIP-Seq)

(Submitter supplied) Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising therapeutics of cancers including prostate cancer. The E3 ubiquitin ligase adaptor protein speckle-type POZ protein (SPOP) is implicated in human prostate cancers due to its frequent mutation. Here we demonstrate that SPOP binds to the BET proteins BRD2, BRD3 and BRD4. Wild-type SPOP, but not prostate cancer-associated mutants, promotes polyubiquitination and proteasome degradation of BET proteins by recognizing a common degron motif. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL11154
10 Samples
Download data: BIGWIG
Series
Accession:
GSE88871
ID:
200088871
7.

SPOP mutation confers intrinsic BET inhibitor resistance in prostate cancer (BRD4_JQ1_RNA-seq)

(Submitter supplied) Bromodomain and extraterminal domain (BET) protein inhibitors are emerging as promising therapeutics of cancers including prostate cancer. The E3 ubiquitin ligase adaptor protein speckle-type POZ protein (SPOP) is implicated in human prostate cancers due to its frequent mutation. Here we demonstrate that SPOP binds to the BET proteins BRD2, BRD3 and BRD4. Wild-type SPOP, but not prostate cancer-associated mutants, promotes polyubiquitination and proteasome degradation of BET proteins by recognizing a common degron motif. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
12 Samples
Download data: BW
8.

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

(Submitter supplied) 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. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
64 Samples
Download data: BW, CSV
9.

RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukemia

(Submitter supplied) Epigenetic pathways regulate gene expression by controlling and interpreting chromatin modifications. Cancer cells are characterized by altered epigenetic landscapes and commonly exploit the chromatin regulatory machinery to enforce oncogenic gene expression programs. While chromatin alterations are, in principle, reversible and often amendable to drug intervention, the promise of targeting such pathways therapeutically has been hampered by our limited understanding of cancer-specific epigenetic dependencies. more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by array
Platforms:
GPL6244 GPL6246
30 Samples
Download data: CEL
Series
Accession:
GSE29799
ID:
200029799
10.

The Short Isoform of BRD4 Promotes HIV-1 Latency by Engaging Repressive SWI/SNF Chromatin Remodeling Complexes

(Submitter supplied) BET proteins commonly activate cellular gene expression, yet inhibiting their recruitment paradoxically reactivates latent HIV-1 transcription. Here we identify the short isoform of BET family member BRD4 (BRD4S) as a novel corepressor of HIV-1 transcription. We found that BRD4S was enriched in chromatin fractions of latently infected T cells and was more rapidly displaced from chromatin upon BET inhibition than the long isoform. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platform:
GPL16791
32 Samples
Download data: WIG, XLSX
11.

iBET resistance

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by array; Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL13112 GPL6887
35 Samples
Download data: BED
Series
Accession:
GSE63683
ID:
200063683
12.

ChIP of BET proteins in iBET resistance [ChIP-seq]

(Submitter supplied) Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers1,2. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
15 Samples
Download data: BED, TXT
Series
Accession:
GSE63682
ID:
200063682
13.

Genome wide expression analysis of BET inhibitor resistance [RNA-seq]

(Submitter supplied) Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers1,2. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13112
6 Samples
Download data: TXT
Series
Accession:
GSE63681
ID:
200063681
14.

Genome wide expression analysis of BET inhibitor resistance

(Submitter supplied) Bromodomain and Extra Terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a new therapeutic paradigm by directly targeting epigenetic readers. Early clinical trials have shown significant promise especially in acute myeloid leukaemia (AML)3; therefore the evaluation of resistance mechanisms, an inevitable consequence of cancer therapies, is of utmost importance to optimise the clinical efficacy of these drugs. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6887
14 Samples
Download data: TXT
Series
Accession:
GSE63575
ID:
200063575
15.

BET Bromodomain Proteins Regulate Transcriptional Reprogramming in Genetic Dilated Cardiomyopathy

(Submitter supplied) In a model of chronic heart failure, BET bromodomain inhibition delayed cardiac remodeling and fibrosis by halting pathologic inflammatory gene networks in an NFkB-dependent manner.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19057
48 Samples
Download data: TXT
Series
Accession:
GSE152005
ID:
200152005
16.

Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
48 Samples
Download data: BED, NARROWPEAK, TXT
Series
Accession:
GSE116919
ID:
200116919
17.

Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (RNAseq)

(Submitter supplied) Three triple negative breast cancer cell lines (MDAMB231, SUM159, and HCC1806) were treated with small molecule inhibitors (JQ1, BET bromodomain inhibitor; GSK2801, BAZ2A/B bromodomain inhibitor) alone and in combination for 72 hours
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: TXT
18.

Response of triple negative breast cancer to BAZ2A/B inhibition and BET bromodomain inhibition alone and in combination (ChIPseq)

(Submitter supplied) Three triple negative breast cancer cell lines (MDAMB231, SUM159, and HCC1806) were treated with small molecule inhibitors (JQ1, BET bromodomain inhibitor; GSK2801, BAZ2A/B bromodomain inhibitor) or BAZ siRNA alone and in combination with JQ1 for 48 hours
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
36 Samples
Download data: BED, NARROWPEAK, XLSX
Series
Accession:
GSE116879
ID:
200116879
19.

BET bromodomain inhibition potentiates ocular melanoma therapy by inducing cell cycle arrest

(Submitter supplied) Ocular melanoma is a common primary malignant ocular tumor in adults with limited effective treatments, so novel therapeutic approaches are desperately needed. Epigenetic regulation plays an important role in tumor development. The SWI/SNF chromatin remodeling complex and bromodomain and extraterminal domain (BET) family proteins are epigenetic regulators involved in several cancers. We aimed to screen a candidate small molecule inhibitor targeting the SWI/SNF complex or BET proteins and investigate its effect and mechanism in ocular melanoma. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
8 Samples
Download data: TXT
Series
Accession:
GSE233589
ID:
200233589
20.

Synthetic lethal and resistance interactions with BET bromodomain inhibitors

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL11154
4 Samples
Download data: H5
Series
Accession:
GSE235793
ID:
200235793
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