Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA177793 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A total of 619 unique promoters were found to be co-targeted by CUL4B and EZH2, among which only 53 were overlapped with the 891 targets of BMI EZH2/PRC2 and CUL4B/CRL4B have a predominant cooperation, at least in KYSE410 cells.
2012-10-17 | GSE41639 | GEO
Project description:<p>BRCA1 mutations are a hallmark of hereditary ovarian cancer, strongly linked to deficiencies in homologous recombination (HR) DNA repair and impaired DNA replication fork protection. However, its roles in cancer progression beyond maintaining genomic integrity remain poorly understood. Through metabolomics approaches, we found BRCA1-deficiency strikingly increased choline metabolism. Loss of BRCA1 promotes choline uptake through upregulating choline transporter-like protein 4 (CTL4). BRCA1 directly binds and recruits EZH2-mediated H3K27Me3 deposition to CTL4 promoter. CTL4 was therefore overexpressed in ovarian cancer tissues with BRCA1 mutations. Furthermore, BRCA1-deficiency significantly promotes ovarian cancer invasion, while inhibition of CTL4 reverses the high metastatic potential of BRCA1-deficient ovarian cancer cells, suggesting the functionality and specificity of CTL4 as a therapeutic target. Additionally, we discovered that phosphocholine, the choline metabolite increased by CTL4 overexpression, interacted with and stabilized the epithelial-to-mesenchymal transition inducer FAM3C in BRCA1-deficient ovarian cancer cells. Importantly, we identified a potent CTL4 inhibitor, DT-13, which significantly reduces choline metabolism and effectively suppresses metastasis in BRCA1-deficient ovarian cancers. Therefore, our study uncovers a mechanism underlying metastasis in BRCA1-deficient cancers and identifies CTL4 as a therapeutic target for metastatic ovarian cancer patients with BRCA1 mutations.</p>
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Project description:ChIP-on-chip from MDA-MB-231 cells with PHF1, CUL4B and PRMT5
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Project description: Not available
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Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
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Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
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Project description:To investigate functional associations between SIRT1 and CUL4B, we used ChIP-seq to analyze genome-wide SIRT1/CUL4B complex transcriptional targets. ChIP experiments were performed first in PANC-1 cells using antibodies against SIRT1 or CUL4B. Next, SIRT1- or CUL4B-associated DNA was amplified using non-biased conditions, labeled, and sequenced. Using Illumina HiSeq2000, we found lots of SIRT1- and CUL4B-specific binding peaks, respectively, representing the ChIP-seq peak. We found that strong enrichment on the promoters of selected genes involved in classical pathways. This study gave us a new understanding of the role of SIRT1/CUL4B in chromatin status and gene transcription.
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Project description:Chip-chip from HepG2 cells with EZH2, SUZ12 and H3K27me3
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