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Links from GEO DataSets

Items: 20

1.

A non-canonical SWI/SNF complex underlies synthetic lethality in cancers driven by BAF complex perturbation

(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
75 Samples
Download data: BW, TXT
Series
Accession:
GSE113042
ID:
200113042
2.

A non-canonical SWI/SNF complex underlies synthetic lethality in cancers driven by BAF complex perturbation [RNA-seq]

(Submitter supplied) Mammalian SWI/SNF chromatin remodeling complexes exist in three distinct, final-form assemblies: canonical BAF (cBAF), PBAF, and a newly characterized non-canonical complex, ncBAF. However, their complex-specific targeting on chromatin, functions and roles in disease remain largely unknown. Here, we comprehensively map complex assemblies on chromatin and find that ncBAF uniquely localizes to CTCF sites and promoters. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
32 Samples
Download data: TXT
3.

A non-canonical SWI/SNF complex underlies synthetic lethality in cancers driven by BAF complex perturbation [ChIP-seq]

(Submitter supplied) Mammalian SWI/SNF chromatin remodeling complexes exist in three distinct, final-form assemblies: canonical BAF (cBAF), PBAF, and a newly characterized non-canonical complex, ncBAF. However, their complex-specific targeting on chromatin, functions and roles in disease remain largely unknown. Here, we comprehensively map complex assemblies on chromatin and find that ncBAF uniquely localizes to CTCF sites and promoters. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
43 Samples
Download data: BW
Series
Accession:
GSE113040
ID:
200113040
4.

SMARCB1 is required for widespread BAF complex-mediated activation of enhancers and bivalent promoters

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing; Other; Expression profiling by high throughput sequencing
Platforms:
GPL11154 GPL18573
78 Samples
Download data: BED, BROADPEAK, NARROWPEAK, TXT
Series
Accession:
GSE90634
ID:
200090634
5.

SMARCB1 is required for widespread BAF complex-mediated activation of enhancers and bivalent promoters [RNA-Seq]

(Submitter supplied) BAF complex perturbations contribute to over 20% of human cancer, yet the mechanisms by which these alterations drive oncogenesis remain poorly understood. The driving role for BAF complex mutations in cancer was first documented in malignant rhabdoid tumor (MRT), an aggressive pediatric cancer in which loss of SMARCB1 (also known as BAF47, INI1, hSNF5), a core BAF complex subunit, is the hallmark genetic alteration. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
12 Samples
Download data: TXT
Series
Accession:
GSE90633
ID:
200090633
6.

SMARCB1 is required for widespread BAF complex-mediated activation of enhancers and bivalent promoters [Hi-C]

(Submitter supplied) BAF complex perturbations contribute to over 20% of human cancer, yet the mechanisms by which these alterations drive oncogenesis remain poorly understood. The driving role for BAF complex mutations in cancer was first documented in malignant rhabdoid tumor (MRT), an aggressive pediatric cancer in which loss of SMARCB1 (also known as BAF47, INI1, hSNF5), a core BAF complex subunit, is the hallmark genetic alteration. more...
Organism:
Homo sapiens
Type:
Other
Platform:
GPL11154
4 Samples
Download data: BED
Series
Accession:
GSE90632
ID:
200090632
7.

SMARCB1 is required for widespread BAF complex-mediated activation of enhancers and bivalent promoters [ChIP-Seq]

(Submitter supplied) BAF complex perturbations contribute to over 20% of human cancer, yet the mechanisms by which these alterations drive oncogenesis remain poorly understood. The driving role for BAF complex mutations in cancer was first documented in malignant rhabdoid tumor (MRT), an aggressive pediatric cancer in which loss of SMARCB1 (also known as BAF47, INI1, hSNF5), a core BAF complex subunit, is the hallmark genetic alteration. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
62 Samples
Download data: BROADPEAK, NARROWPEAK, XLSX
Series
Accession:
GSE90631
ID:
200090631
8.

BRD9 defines a novel SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors [RNA-seq 2]

(Submitter supplied) Bromodomain-containing protein 9 (BRD9) was recently identified to be associated with the chromatin remodeling SWI/SNF(BAF) complex, yet its function within the complex has remained unclear. Here, using genome-scale CRISPR-Cas9 screens, we found that BRD9 constitutes a specific vulnerability in highly malignant pediatric rhabdoid tumors, which are driven by inactivating mutations of SMARCB1 subunit of SWI/SNF complexes. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
16 Samples
Download data: TXT
9.

BRD9 defines a novel SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors

(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
31 Samples
Download data: BW, TXT
Series
Accession:
GSE120235
ID:
200120235
10.

BRD9 defines a novel SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors [ChIP-seq]

(Submitter supplied) Bromodomain-containing protein 9 (BRD9) was recently identified to be associated with the chromatin remodeling SWI/SNF(BAF) complex, yet its function within the complex has remained unclear. Here, using genome-scale CRISPR-Cas9 screens, we found that BRD9 constitutes a specific vulnerability in highly malignant pediatric rhabdoid tumors, which are driven by inactivating mutations of SMARCB1 subunit of SWI/SNF complexes. more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL18573
11 Samples
Download data: BW
Series
Accession:
GSE120234
ID:
200120234
11.

BRD9 defines a novel SWI/SNF sub-complex and constitutes a specific vulnerability in malignant rhabdoid tumors [RNA-seq]

(Submitter supplied) Bromodomain-containing protein 9 (BRD9) was recently identified to be associated with the chromatin remodeling SWI/SNF(BAF) complex, yet its function within the complex has remained unclear. Here, using genome-scale CRISPR-Cas9 screens, we found that BRD9 constitutes a specific vulnerability in highly malignant pediatric rhabdoid tumors, which are driven by inactivating mutations of SMARCB1 subunit of SWI/SNF complexes. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18573
4 Samples
Download data: TXT
12.

Structural and functional properties of mSWI/SNF chromatin remodeling complexes revealed through single-cell perturbation and genomic profiling

(Submitter supplied) Mammalian SWI/SNF (mSWI/SNF or BAF) chromatin remodeling complexes play critical roles in regulating DNA accessibility and gene expression and are comprised of three final-form assemblies, cBAF, PBAF, and ncBAF, which exhibit distinct modular organization, chromatin targeting, and roles in disease. However, the contributions of each subcomplex and their constituent subunits to gene expression remain incompletely defined. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing; Other
Platforms:
GPL18573 GPL15520 GPL16791
38 Samples
Download data: CSV, MTX, TSV
Series
Accession:
GSE200201
ID:
200200201
13.

BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...
Organism:
Homo sapiens; Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL24676 GPL24247
10 Samples
Download data: BW, TXT
Series
Accession:
GSE236960
ID:
200236960
14.

BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state [Mouse_Brd9_CTCF ChIP-seq]

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: BW
Series
Accession:
GSE236959
ID:
200236959
15.

BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state [MOLM13 DMSO vs dBRD9 RNA-seq]

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: TXT
Series
Accession:
GSE236958
ID:
200236958
16.

BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state [mouse_Brd9_H3K27Ac-ChIP-seq]

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: BIGWIG
Series
Accession:
GSE236330
ID:
200236330
17.

BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state [mouse_Brd9_ATAC-seq]

(Submitter supplied) Chromatin remodeling caused by SWI/SNF (BAF) complexes is essential for regulating cell fates. Of these, BRD9, an essential component of the non-canonical BAF (ncBAF) complex, is post-transcriptionally decayed in multiple types of cancer, especially in myelodysplastic syndrome (MDS). However, how BRD9 loss or ncBAF disruption alters the HSCs' integrity remains unknown. Here, we identify that Brd9 loss enhances chromatin accessibility, promoting myeloid-lineage skewing at the expense of B cell development in vivo, followed by MDS development. more...
Organism:
Mus musculus
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24247
4 Samples
Download data: BIGWIG
Series
Accession:
GSE236329
ID:
200236329
18.

BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state [human_Brd9_CTCF-ChIP-seq]

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
4 Samples
Download data: BIGWIG
Series
Accession:
GSE236328
ID:
200236328
19.

BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state [human_Brd9_bulkRNA-seq]

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: TXT
Series
Accession:
GSE236327
ID:
200236327
20.

BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state [human_Brd9_ATAC-seq]

(Submitter supplied) Switch/sucrose nonfermentable (SWI/SNF) complexes are ATP-dependent chromatin remodeler complexes that play critical roles in timely and appropriate gene regulation by modulating chromatin architecture and DNA accessibility. SWI/SNF complexes can be grouped into three subcomplexes of differing sizes, canonical BAF (cBAF), polybromo BAF (PBAF), and newly identified noncanonical BAF (ncBAF). The most recently characterized ncBAF lacks the core BAF subunits ARID, BAF47, and BAF57, but includes unique subunits GLTSCR1/1L and BRD9, one of the bromodomain-containing proteins.We recently demonstrated the novel mechanism for the ncBAF disruption caused by mutations in a spiceosomal protein, SF3B1, especially in 65–83% for myelodysplastic syndromes (MDS) with ring sideroblasts as well as in >20% of mucosal/uveal melanomas, suggesting that the disturbed ncBAF may have some roles in the malignant hematopoiesis.Mechanistically, SF3B1 mutant recognizes an aberrant, deep intronic branchpoint within BRD9 and thereby induces the inclusion of an aberrant exon and subsequently profound degradation of BRD9 mRNA by triggering nonsense-mediated RNA decay (NMD). more...
Organism:
Homo sapiens
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL24676
6 Samples
Download data: BIGWIG
Series
Accession:
GSE236326
ID:
200236326
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