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BCLAF1 Chip-chip control (siGFP) and BRCA1 depleted (siBRCA1) 293T cells in the absense or presense of Etoposide

ABSTRACT: BCLAF1 is a serine-arginine (SR) protein implicated in transcriptional regulation and mRNA splicing. We have recently identified BCLAF1 as part of a novel mRNA splicing complex that is recruited to different genetic promoters by the breast cancer susceptiblity protein, BRCA1 in response to DNA damage. This ChIP-chip study was designed to identify genes/promoters regulated by the BRCA1/BCLAG1 mRNA splicing complex by identifying promoters bound by BCLAF1 in the absense and presense of BRCA1 in control cells and cells treated with etoposide to induce DNA damage. This study includes tripicate BCLAF1 ChIP-chip experiments in untreated and etoposide treated (1uM 16 hours) control cells (siGFP) and cells depleted of BRCA1 (siBRCA1).

ORGANISM(S): Homo sapiens

PROVIDER: GSE47016 | GEO | 2014/04/25

SECONDARY ACCESSION(S): PRJNA203287

REPOSITORIES: GEO

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BCLAF1 Chip-chip control (siGFP) and BRCA1 depleted (siBRCA1) 293T cells in the absense or presense of Etoposide

Project description:BCLAF1 is a serine-arginine (SR) protein implicated in transcriptional regulation and mRNA splicing. We have recently identified BCLAF1 as part of a novel mRNA splicing complex that is recruited to different genetic promoters by the breast cancer susceptiblity protein, BRCA1 in response to DNA damage. This ChIP-chip study was designed to identify genes/promoters regulated by the BRCA1/BCLAG1 mRNA splicing complex by identifying promoters bound by BCLAF1 in the absense and presense of BRCA1 in control cells and cells treated with etoposide to induce DNA damage. This study includes tripicate BCLAF1 ChIP-chip experiments in untreated and etoposide treated (1uM 16 hours) control cells (siGFP) and cells depleted of BRCA1 (siBRCA1). Chromatin Immunoprecipitaitons were performed in triplicate with BCLAF1 antibodies in control 293T cells transfected with siGFP siRNAs and BRCA1 siRNAs (siBRCA1 to deplete BRCA1). Immunoprecipitated genomic DNA was labelled with Cy3 and Input genomic DNA was labelled with Cy5 and hybridized to NimbleGen human 3x720k RefSeq promoter arrays to identify BCLAF1 boundgenomic DNA regions.

2014-04-25 | E-GEOD-47016 | biostudies-arrayexpress

Homo sapiens

Project description:BCLAF1 Chip-chip control (siGFP) and BRCA1 depleted (siBRCA1) 293T cells in the absense or presense of Etoposide

| PRJNA203287 | ENA

Expression data after BCLAF1-L knockdown in human RKO cells

Project description:Bcl-2-accociated transcription factor 1(BCLAF1) has been reported to be involved in diverse biological processes. Alternative splicing leads to mutiple transcript virants in human cells and we are interested in functions of its full length isoform(BCLAF1-L) in human colon cancer cells, thus to understanding its role in colon cancer progression. We used microarray to detail the global programme of gene expression after BCLAF1-L knockdown(sh-BCLAF1-L#1) in RKO cells and identified distinct classes of up-regulated or down-regulated genes impaired by its inhibition, when comparing with the control group(sh-Luci). RKO cells were infected with retroviruses either expressing control (sh-Luci) or BCLAF1-L knockdown (sh-BCLAF1-L#1). Medium was replaced 24h after infection, and infected cells were selected by the addition of puromycin (2ug/ml) for 72-96h. Then cells were havested for RNA extraction and hybridization on Affymetrix microarrays.

2013-12-05 | E-GEOD-52990 | biostudies-arrayexpress

Expression data after BCLAF1-L knockdown in human RKO cells

2013-12-05 | GSE52990 | GEO

BCLAF1 and its pre-mRNA splicing regulator SRSF10 both regulate tumorigenic capacity of human colon cancer cells

Project description:Bcl-2-accociated transcription factor 1(BCLAF1) has been shown to be involved in multiple biological processes. Transcript variants encoding different isoforms that are generated by alternative splicing have been found for this gene, but little is known about the mechanisms governing its splicing regulation and whether the misregulation is associated with cancer development. Mechanistic analysis revealed that splicing factor SRSF10 specifically interacts with exon5a and activates its inclusion, as RNAi-mediated knockdown of SRSF10 induced a dramatic skipping of exon5a. To define a comprehensive programm of alternative splicing that is regulated by SRSF10 in RKO cells, we used RNA-seq coupled with a bioinformatic analysis to identify the extensive splicing network regulated by SRSF10 in RKO cells.

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The miR-194-5p/BCLAF1 module is responsible for maturation block, cell fate and treatment susceptibility in AML.

Project description:miRNAs deregulation contributes to cancer. miR-194-5p is up-regulated by the HDAC inhibitor (HDACi) SAHA, negatively modulating BCL2-associated transcription factor 1 (BCLAF1). We prove that the miR-194-5p/BCLAF1 equilibrium regulates differentiation, survival and self-renewal of normal progenitors and acute myeloid leukemia (AML) blasts. This equilibrium is perturbed in AMLs resulting in highly expressed BCLAF1, suppression of miR194-5p, consequently, locking cells into an immature, potentially ‘immortal’ state. HDACis reverse this scenario relocating BCLAF1 from the nucleus to a peri-membrane ring-like cytoplasmic structure, sensitizing the cells to differentiation or apoptosis. miR-194-5p and BCLAF1 are significantly deregulated in a cohort of 60 primary AMLs and get restored by HDACi. Our findings connect responsiveness to treatment to re-instatement of miR-194-5p/BCLAF1 balance. These findings might be exploited for (epi-based) anti-leukemia therapy.

2017-12-20 | GSE76426 | GEO

Gene expression profiling in Bclaf1 deficient versus wild type post natal day1 lung

Project description:In this study we compared the gene expression pattern in Bclaf1-deficient vs wild type lung tissue Keywords: Gene expression profiling

2007-09-15 | GSE9034 | GEO

Mediator MED23 induces premature senescence by interacting with BCLAF1 via blocking autophagy flux in lung cancer cells

Project description:macroautophagy/autophagy plays a key role in regulating the balance between cell survival and senescence during the progression of lung cancer. Med23 (also known as Sur2), a protein belonging to an evolutionarily conserved high-molecularmass complex composed of more than 20 distinct subunits, promotes the growth, metastasis , and migration of lung cancer cells and is overexpressed in multiple cancers. However, the function of MED23 in autophagy regulation remains unknown. Here, we observes that MED23 expression is significantly upregulated in a subset of cancer cells and reversely correlated with overall survival rates and clinical stage for lung cancer patients. Mechanistically, MED23 is found to interact with BCLAF1 (BCL-2-associated transcription factor 1, BTF) ,a nuclear protein that can induce apoptosis and autophagy. Moreover, BCLAF1 interacts with the promoter of NUPR1 and downregulates its expression. We further show that BCLAF1 and MED23 depletion inhibits autophagy and induces premature senescence in vitro. Remarkably, the expression of BCLAF1 and MED23 are negatively correlated with NUPR1 in the human lung cancer tissues and adjacent normal tissues. Collectively, our data reveal a physical and genetic interaction between BCLAF1 and MED23, suggesting that MED23 constitutes a molecular node in the regulatory network of autophagy and this pathway may be an important therapeutic target in lung cancer.

2019-12-23 | GSE142508 | GEO

Identifying and characterising Thrap3, Bclaf1 and Erh direct interactions using cross-linking mass spectrometry

Project description:Cross-linking mass spectrometry (XL-MS) is a powerful technology capable of yielding structural insights across the complex cellular protein interaction network. We performed XL-MS using MS-cleavable cross-linker disuccinimidyl sulfoxide (DSSO) on endogenous affinity-purified BAF complex. We identified numerous crosslinks between three BAF co-purifying proteins, namely Thrap3, Bclaf1 and Erh. Our data suggests that Bclaf1, Erh and Thrap3 interact closely and might represent a stable complex. The XL data allowed us to map interaction surfaces on Thrap3 and B, which overlap with the non-disordered portions of both proteins.

2021-09-24 | PXD027611 | Pride

Mll3/Mll4 catalytic activity is necessary for de novo enhancer-promoter contacts during embryonic stem cell differentiation [PLAC-seq]

Project description:PLAC-seq, mRNA-seq, and ChIP-seq experiments in mouse embryonic stem cells and neural progenitor cells in the presense or absence of Mll3/4 catalytic activity.

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