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Links from GEO DataSets

Items: 20

1.

MUC1-C INDUCES PBRM1-MEDIATED CHROMATIN REMODELING IN DRIVING CHRONIC INFLAMMATION AND DNA DAMAGE RESISTANCE IN TRIPLE-NEGATIVE BREAST CANCER

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
18 Samples
Download data
Series
Accession:
GSE212170
ID:
200212170
2.

MUC1-C INDUCES PBRM1-MEDIATED CHROMATIN REMODELING IN DRIVING CHRONIC INFLAMMATION AND DNA DAMAGE RESISTANCE IN TRIPLE-NEGATIVE BREAST CANCER [tet-MUC1 shRNA]

(Submitter supplied) STAT1 and IRF1 are essential effectors of the type I and II interferon (IFN) pathways. Here, we report that the oncogenic MUC1-C protein is necessary for inducing chromatin accessibility and activation of the STAT1 and IRF1 genes in triple-negative breast cancer (TNBC) cells. Our results demonstrate that MUC1-C activates the PBRM1 subunit of the SWI/SNF PBAF chromatin remodeling complex and forms a nuclear complex with PBRM1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: CSV
Series
Accession:
GSE212587
ID:
200212587
3.

MUC1-C INDUCES PBRM1-MEDIATED CHROMATIN REMODELING IN DRIVING CHRONIC INFLAMMATION AND DNA DAMAGE RESISTANCE IN TRIPLE-NEGATIVE BREAST CANCER [BT549_shPBRM1]

(Submitter supplied) STAT1 and IRF1 are essential effectors of the type I and II interferon (IFN) pathways. Here, we report that the oncogenic MUC1-C protein is necessary for inducing chromatin accessibility and activation of the STAT1 and IRF1 genes in triple-negative breast cancer (TNBC) cells. Our results demonstrate that MUC1-C activates the PBRM1 subunit of the SWI/SNF PBAF chromatin remodeling complex and forms a nuclear complex with PBRM1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: CSV
Series
Accession:
GSE212169
ID:
200212169
4.

MUC1-C INDUCES PBRM1-MEDIATED CHROMATIN REMODELING IN DRIVING CHRONIC INFLAMMATION AND DNA DAMAGE RESISTANCE IN TRIPLE-NEGATIVE BREAST CANCER [BT549_shIRF1]

(Submitter supplied) STAT1 and IRF1 are essential effectors of the type I and II interferon (IFN) pathways. Here, we report that the oncogenic MUC1-C protein is necessary for inducing chromatin accessibility and activation of the STAT1 and IRF1 genes in triple-negative breast cancer (TNBC) cells. Our results demonstrate that MUC1-C activates the PBRM1 subunit of the SWI/SNF PBAF chromatin remodeling complex and forms a nuclear complex with PBRM1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: CSV
Series
Accession:
GSE212168
ID:
200212168
5.

Muc1-C Induces Pbrm1-Mediated Chromatin Remodeling in Driving Chronic Inflammation and DNA Damage Resistance in Triple-Negative Breast Cancer

(Submitter supplied) STAT1 and IRF1 are essential effectors of the type I and II interferon (IFN) pathways. Here, we report that the oncogenic MUC1-C protein is necessary for inducing chromatin accessibility and activation of the STAT1 and IRF1 genes in triple-negative breast cancer (TNBC) cells. Our results demonstrate that MUC1-C activates the PBRM1 subunit of the SWI/SNF PBAF chromatin remodeling complex and forms a nuclear complex with PBRM1. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
18 Samples
Download data: CSV
Series
Accession:
GSE206212
ID:
200206212
6.

MUC1-C integrates activation of the IFN-γ pathway with suppression of the tumor immune microenvironment in triple-negative breast cancer

(Submitter supplied) Immune checkpoint inhibitors (ICIs) have had a profound impact on the treatment of many tumors; however, their effectiveness against triple-negative breast cancers (TNBCs) has been limited. One factor limiting responsiveness of TNBCs to ICIs is a lack of functional tumor i-infiltrating lymphocytes (TILs) in ‘“non-inflamed’” or ‘“cold’” tumor immune microenvironments (TIMEs), albeitalthough by unknown mechanisms. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
6 Samples
Download data: CSV
7.

MUC1-C INTEGRATES CHRONIC TYPE II INTERFERON SIGNALING WITH CHROMATIN REMODELING PATHWAYS IN IMMUNOSUPPRESSION OF PROSTATE CANCER

(Submitter supplied) The cancer stem cell (CSC) state is intimately associated with suppression of the immune tumor microenvironment (TME). The oncogenic MUC1-C protein drives dedifferentiation of castrate resistant prostate cancer (CRPC) CSCs in association with induction of the BAF, NuRD and PBAF chromatin remodeling complexes. The present work demonstrates that MUC1-C is necessary for expression of IFNGR1 and activation of the type II interferon-gamma (IFN- pathway in CRPC cells. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: CSV
8.

MUC1-C Drives Lineage Plasticity in Progression to Neuroendocrine Prostate Cancer

(Submitter supplied) Neuroendocrine prostate cancer (NEPC) is a highly aggressive malignancy of increasing prevalence with an unmet need for targeted therapeutic approaches. The oncogenic MUC1-C protein is overexpressed in castration-resistant prostate cancer (CRPC) and NEPC; however, there is no known role for MUC1-C in driving lineage plasticity to these advanced PC phenotypes. The present studies demonstrate that upregulation of MUC1-C in androgen-independent (AI) PC cells suppresses androgen receptor (AR) axis signaling and induces the neural BRN2 transcription factor by a previously unrecognized MYC-mediated mechanism. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: CSV
9.

MUC1-C DICTATES JUN AND BAF-MEDIATED CHROMATIN REMODELING AT PROMOTER AND ENHANCER SIGNATURES IN CANCER STEM CELLS

(Submitter supplied) We report the application of ATAC-seq to study the role of MUC1-C in chromatin remodeling in cancer stem cells
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: NARROWPEAK, TXT
Series
Accession:
GSE180599
ID:
200180599
10.

MUC1-C ACTIVATES THE NURD COMPLEX IN DEDIFFERENTIATION OF TRIPLE-NEGATIVE BREASTCANCER CELLS

(Submitter supplied) The NuRD chromatin remodeling and deacetylation complex, which includes MTA1, MBD3, CHD4 and HDAC1 among other components, is of importance for development and cancer progression. The oncogenic MUC1-C protein activates EZH2 and BMI1 in the epigenetic reprogramming of triple-negative breast cancer (TNBC) cells. However, there is no known link between MUC1-C and chromatin remodeling complexes. The present studies demonstrate that MUC1-C binds directly to the MYC HLH/LZ domain. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: CSV
11.

The effects of PBRM1 loss on the ccRCC transcriptome

(Submitter supplied) Subunits of SWI/SNF chromatin remodeling complexes are frequently mutated in human malignancies. The PBAF complex is composed of multiple subunits, including the tumor suppressor protein PBRM1 (BAF180), as well as ARID2 (BAF200), that are unique to this SWI/SNF complex. PBRM1 is mutated in various cancers, with a high mutation frequency in clear cell renal cell carcinoma (ccRCC). In this study, we integrate RNA-seq, histone modification ChIP-seq, and ATAC-seq data to show that loss of PBRM1 results in de novo gains in H3K4me3 peaks throughout the epigenome including activation of a retinoic acid biosynthesis and signaling gene signature. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
18 Samples
Download data: SF
Series
Accession:
GSE196129
ID:
200196129
12.

Genome-wide maps of histone modification and chromatin remodeler binding in mouse calvaria derived stromal cell line (OP9)

(Submitter supplied) We have used chromatin immunoprecipitation followed by high throughput sequencing to map regions of chromatin remodeler and histone modification state. We have used this data to understand the global distribution in stromal cell and probable mechanism of transcriptional regulation.
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL17021
14 Samples
Download data: BW
Series
Accession:
GSE139216
ID:
200139216
13.

Genome-wide chromatin profiles of PBRM1 Drug treatment [RNA-Seq]

(Submitter supplied) PBRM1 encodes an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler and the inactivation of PBRM1 is the second most frequent mutational event in kidney cancer. However, the impact of PBRM1 loss on chromatin remodeling, especially pertaining to kidney tumorigenesis, has not been well examined. Here we show that in VHL-deficient renal tumors, PBRM1 deficiency results in aberrant PBAF complexes that localize to de novo genomic loci and activate the pro-tumorigenic NF-κB pathway. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
20 Samples
Download data: TXT
Series
Accession:
GSE222245
ID:
200222245
14.

Genome-wide chromatin profiles of PBRM1 Drug treatment [ChIP-Seq]

(Submitter supplied) PBRM1 encodes an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler and the inactivation of PBRM1 is the second most frequent mutational event in kidney cancer. However, the impact of PBRM1 loss on chromatin remodeling, especially pertaining to kidney tumorigenesis, has not been well examined. Here we show that in VHL-deficient renal tumors, PBRM1 deficiency results in aberrant PBAF complexes that localize to de novo genomic loci and activate the pro-tumorigenic NF-κB pathway. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
32 Samples
Download data: NARROWPEAK
Series
Accession:
GSE222244
ID:
200222244
15.

Genome-wide chromatin profiles of PBRM1

(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
5 related Platforms
170 Samples
Download data: BED, NARROWPEAK
Series
Accession:
GSE152735
ID:
200152735
16.

Genome-wide chromatin profiles of PBRM1 [RNA-Seq]

(Submitter supplied) PBRM1 is an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler. The inactivation of PBRM1 is the second most frequent mutational event in kidney tumorigenesis. Here we show that in VHL-deficient ccRCC tumors, PBRM1 loss results in an altered PBAF complex that retains the association between SMARCA4 and ARID2 but disengages BRD7 from SMARCA4. The PBRM1-deficient PBAF complexes redistribute from promoter proxy regions to distal enhancer regions. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL20795 GPL24676
41 Samples
Download data: TXT
Series
Accession:
GSE152734
ID:
200152734
17.

Genome-wide chromatin profiles of PBRM1 [ChIP-Seq]

(Submitter supplied) PBRM1 encodes an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler and the inactivation of PBRM1 is the second most frequent mutational event in kidney cancer. However, the impact of PBRM1 loss on chromatin remodeling, especially pertaining to kidney tumorigenesis, has not been well examined. Here we show that in VHL-deficient renal tumors, PBRM1 deficiency results in aberrant PBAF complexes that localize to de novo genomic loci and activate the pro-tumorigenic NF-?B pathway. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL20301 GPL16791
77 Samples
Download data: BED
Series
Accession:
GSE152681
ID:
200152681
18.

Pbrm1 regulates interferon signaling in mouse AML

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens; Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing
Platforms:
GPL24676 GPL24247
26 Samples
Download data: BW, NARROWPEAK, TXT
Series
Accession:
GSE211263
ID:
200211263
19.

Pbrm1 regulates interferon signaling in mouse AML [RNA-seq HAP1]

(Submitter supplied) CRISPR/Cas9 screening approaches are powerful tools to identify in vivo cancer dependencies. Hematopoietic malignancies are genetically complex disorders in which sequential acquisition of somatic mutations generates clonal diversity. With time, additional cooperating mutations may drive disease progression. Using an in vivo pooled gene editing screen of epigenetic factors in primary murine hematopoietic stem and progenitor cells (HSPCs), we sought to uncover unrecognized genes that contribute to leukemia progression. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
12 Samples
Download data: TXT
Series
Accession:
GSE211262
ID:
200211262
20.

Pbrm1 regulates interferon signaling in mouse AML [RNA-seq Mouse]

(Submitter supplied) CRISPR/Cas9 screening approaches are powerful tools to identify in vivo cancer dependencies. Hematopoietic malignancies are genetically complex disorders in which sequential acquisition of somatic mutations generates clonal diversity. With time, additional cooperating mutations may drive disease progression. Using an in vivo pooled gene editing screen of epigenetic factors in primary murine hematopoietic stem and progenitor cells (HSPCs), we sought to uncover unrecognized genes that contribute to leukemia progression. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
9 Samples
Download data: TXT
Series
Accession:
GSE211261
ID:
200211261
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