Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from Knockdown of BAF53A in DLD1 cell line

ABSTRACT: BAF53A, an important subunit of the SWI/SNF epigenetic chromatin regulatory complex, has been implicated as the driver of diverse cancers. However, the role of BAF53A in colorectal cancer (CRC) remains poorly understood.

ORGANISM(S): Homo sapiens

PROVIDER: GSE218008 | GEO | 2022/12/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Baf53a is involved in survival of mouse ES cells, which can be compensated by Baf53b.

Project description:The human Baf (Brg1/Brm associated factor) complex, also known as the mammalian SWI/SNF chromatin-remodeling complex, is involved in a variety of cellular processes. The pluripotency and self-renewal abilities are major characteristics of embryonic stem (ES) cells and are regulated by the ES cell-specific BAF (esBAF) complex. Baf53a is one of the subunits of the esBAF complex. Here, we found that growth of Baf53a-deficient ES cells was repressed, and expression of p53, p21, and cleaved Caspase 3 was increased. Interestingly, Baf53b, a homologue of Baf53a, rescued cell death of Baf53a-deficient ES cells. Baf53a-deficient ES cells overexpressing exogenous Baf53a or Baf53b remained in the undifferentiated state and proliferated. In summary, our findings suggest that Baf53a is involved in the survival of ES cells, and that Baf53b is able to compensate for this functional aspect of Baf53a.

2017-11-16 | GSE103694 | GEO

Expression data from Knockdown of BAF53A in DLD1 cell line

Project description:Expression data from Knockdown of BAF53A in DLD1 cell line

| PRJNA901907 | ENA

Loss of Snf5 and the formation of an aberrant SWI/SNF complex

Project description:Aberrant forms of the SWI/SNF chromatin remodeling complex are associated with human disease. Loss of the Snf5 subunit of SWI/SNF is a driver mutation in pediatric rhabdoid cancers and forms aberrant sub-complexes that are not well characterized. We determined the effects of loss of Snf5 on the composition, nucleosome binding, recruitment and remodeling activities of yeast SWI/SNF. The Snf5 subunit interacts with the ATPase domain of Snf2 and forms a submodule consisting of Snf5, Swp82 and Taf14 as shown by mapping SWI/SNF subunit interactions by crosslinking-mass spectrometry and subunit deletion followed by immunoaffinity chromatography. Snf5 promoted binding of the Snf2 ATPase domain to nucleosomal DNA, enhanced its catalytic activity and facilitated nucleosome remodeling. Snf5 was required for acidic transcription factors to recruit SWI/SNF to chromatin. RNA-seq analysis suggested that both the recruitment and catalytic functions mediated by Snf5 are required for SWI/SNF regulation of gene expression.

2017-01-30 | GSE85460 | GEO

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [CnR]

Project description:To determine whether the chromatin accessibility for YAP/TEADs in squamous cell carcinoma cells is directly regulated by BAF53A within BAF complexes, we performed CUT&RUN to profile the distribution of YAP, TEAD1, and BAF155 (a DNA binding subunit of BAF complexes) across the genome.

2021-10-29 | GSE156787 | GEO

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [RNA-seq]

Project description:To identify genes regulated by BAF53A, we carried out RNA-seq analysis in three SCC cell lines after BAF53A knockdown by siRNA and in normal keratinocytes with BAF53A overexpression.

2021-10-29 | GSE156785 | GEO

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [ATAC-seq]

Project description:To identify accessible chromatin regions regulated BAF53A in squamous cell carcinomas (SCCs), we performed ATAC-seq in FaDu SCC cell lines after BAF53A knockdown by siRNA and in normal keratinocytes with BAF53A overexpression.

2021-10-29 | GSE156786 | GEO

siRNA Knockdown of SWI/SNF complex proteins in prostate cancer cell lines

Project description:Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus siRNAs targeting SWI/SNF complex proteins (SMARCA2, SMARCA4, and SMARCB1). Goal was to determine the effect of SWI/SNF knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SWI/SNF-siRNA treated cells. Three SWI/SNF proteins were targeted: SMARCA2, SMARCA4, and SMARB1. Biological replicates: 1 control replicate, 2 treatment replicates per SWI/SNF protein. Technical replicates: 1 replicate per SWI/SNF protein. Cell lines: 22Rv1 and LNCaP.

2013-07-20 | E-GEOD-40384 | biostudies-arrayexpress

SWI/SNF inhibition leads to epigenetic reprogramming in rhabdoid tumor [ChIP-seq]

Project description:Rhabdoid tumor is a pediatric cancer characterized by the biallelic inactivation of SMARCB1, a subunit of the SWI/SNF chromatin remodeling complex. SMARCB1 inactivation leads to SWI/SNF redistribution to favor a proliferative dedifferentiated cellular state. Although this deletion is the known oncogenic driver, SWI/SNF therapeutic targeting remains a challenge. Here we show mithramycin and a second-generation analogue EC-8042 are effective in this tumor type. Mithramycin evicts SWI/SNF from chromatin triggering a cellular response characterized by chromatin compartment remodeling and promoter reprogramming. These effects lead to differentiation and marked xenograft tumor regressions in vivo. This study provides a therapeutic candidate for rhabdoid tumor and an approach that may be applicable to the more than 20% of cancers characterized by mutated SWI/SNF.

2020-11-16 | GSE137399 | GEO

SWI/SNF inhibition leads to epigenetic reprogramming in rhabdoid tumor [ATAC-seq]

2020-11-16 | GSE137397 | GEO

SWI/SNF inhibition leads to epigenetic reprogramming in rhabdoid tumor [RNA-seq]

2020-11-16 | GSE137403 | GEO