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Total mRNA-seq to determine how the gene expression is altered in both parental and BRCA2-depleted CCNC- and MED12-KO cells.

ABSTRACT: Total mRNA-seq to determine how the gene expression is altered in both parental and BRCA2-depleted CCNC- and MED12-KO cells.

PROVIDER: PRJNA631017 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11729346_1.fastq.gz	Fastqsanger.gz
	SRR11729346_2.fastq.gz	Fastqsanger.gz
	SRR11729347_1.fastq.gz	Fastqsanger.gz
	SRR11729347_2.fastq.gz	Fastqsanger.gz
	SRR11729348_1.fastq.gz	Fastqsanger.gz

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Total mRNA-seq to determine how the gene expression is altered in both parental and BRCA2-depleted CCNC- and MED12-KO cells.

Project description:Background: Loss of RNA Pol II transcription Mediator components like CCNC, MED12 led to improved survival of PARPi-treated and untreated BRCA2-depleted cells. Mediator is best known for its function with RNA Pol II in regulating gene transcription, we performed total mRNA-Seq with control and BRCA2-depleted CCNC- and MED12-KO cells. The aim of the present prospective study was to reveal how the gene expression is altered in both parental and BRCA2-depleted CCNC- and MED12-KO cells which might contribute to the PARPi resistance in BRCA2 depleted cells. Methods: HEK293A BRCA2 CKI mAID-EGFP WT, CCNC-KO, and MED12-KO with or without BRCA2 depletion cells (each with two biological replicates) were collected and total RNA was extracted and subjected to RNA-seq at HiSeq3000 (Illumina). Results: Based on the transcriptomic data, we examined differentially expressed genes and performed KEGG pathway enrichment analysis.The results suggested that in both control and BRCA2-depleted CCNC- and MED12-knockout cells, several signaling pathways like the transforming growth factor (TGF)-beta signaling pathway and extracellular matrix (ECM)-receptor interaction pathway et al were activated which probably facilitate cell proliferation upon BRCA2 loss. Conclusions: Our results imply that TGF-beta signaling and other signaling pathways such as the ECM-receptor interaction pathway which play roles in the regulation of cellular functions such as proliferation, adhesion, apoptosis, differentiation and migration, may together contribute to the involvement of CCNC and MED12 in drug resistance.

2021-05-06 | GSE150067 | GEO

Determination of MED12 protein interactome

Project description:Here, the goal of our study was to determine the protein-protein interactome of MED12 in resting and activated human T-cells. We immunoprecipitated endogenous MED12 and evaluated the protein interactome in comparison to an isotype-matched IgG as a control.

2024-12-05 | PXD056255 | Pride

Germline BRCA2 mutations drive prostate cancers with distinct evolutionary trajectories

Project description:Germline mutations in the BRCA2 tumour suppressor are associated with both an increased lifetime risk of developing prostate cancer (PCa) and increased risk of aggressive disease. To understand this aggression, here we profile the genomes and methylomes of localized PCa from 14 carriers of deleterious germline BRCA2 mutations (BRCA2-mutant PCa). We show that BRCA2-mutant PCa harbour increased genomic instability and a mutational profile that more closely resembles metastastic than localized disease. BRCA2-mutant PCa shows genomic and epigenomic dysregulation of the MED12L/MED12 axis, which is frequently dysregulated in metastatic castration-resistant prostate cancer (mCRPC). This dysregulation is enriched in BRCA2-mutant PCa harbouring intraductal carcinoma (IDC). Microdissection and sequencing of IDC and juxtaposed adjacent non-IDC invasive carcinoma in 10 patients demonstrates a common ancestor to both histopathologies. Overall we show that localized castration-sensitive BRCA2-mutant tumours are uniquely aggressive, due to de novo aberration in genes usually associated with metastatic disease, justifying aggressive initial treatment.

2017-01-10 | GSE80685 | GEO

RNA expression in BRCA2-depleted breast cancer cell lines

Project description:Next generation RNA sequencing was performed to analyze changes in gene expression upon BRCA2 depletion. BRCA2 depletion was introduced in two human breast cancer cell lines with doxycyclin inducible short hairpin RNAs.

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Med12 and p300 chips in HSPCs

Project description:We characterized the genome wide occupancy of Med12 and p300 in mouse HSPCs. We also characterize p300 occupancy upon shRNA against control or Med12. ChIP-seq analysis of Med12 and/or p300 in untreated HSPCs

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Effects of BRCA2 cis-regulation in normal breast and cancer risk amongst BRCA2 mutation carriers

Project description:This SuperSeries is composed of the following subset Series: GSE32124: Effects of BRCA2 cis-regulation in normal breast and cancer risk amongst BRCA2 mutation carriers [expression data] GSE32258: Effects of BRCA2 cis-regulation in normal breast and cancer risk amongst BRCA2 mutation carriers [SNP data] Refer to individual Series

2012-02-01 | E-GEOD-32259 | biostudies-arrayexpress

Med12 and p300 chips in HSPCs

Project description:We characterized the genome wide occupancy of Med12 and p300 in mouse HSPCs. We also characterize p300 occupancy upon shRNA against control or Med12.

2016-08-25 | GSE76053 | GEO

BRCA2 ChIP-seq hTert-HME1 cell line

Project description:Individuals with a single functional copy of the BRCA2 tumor suppressor have elevated risks for breast, ovarian, and other solid tumor malignancies. The exact mechanisms of carcinogenesis due to BRCA2 haploinsufficiency remain unclear, but one possibility is that at-risk cells are subject to acute periods of decreased BRCA2 availability and function ("BRCA2-crisis"), which may contribute to disease. Here, we establish an in vitro model for BRCA2-crisis that demonstrates chromatin remodeling and activation of an NF-κB survival pathway in response to transient BRCA2 depletion. Mechanistically, we identify BRCA2 chromatin binding, histone acetylation, and associated transcriptional activity as critical determinants of the epigenetic response to BRCA2-crisis. These chromatin alterations are reflected in transcriptional profiles of pre-malignant tissues from BRCA2 carriers and, therefore, may reflect natural steps in human disease. By modeling BRCA2-crisis in vitro, we have derived insights into pre-neoplastic molecular alterations that may enhance the development of preventative therapies.

2019-08-07 | GSE133450 | GEO

Genome-wide characterization of MED12 occupancy in human CD34+ cells

Project description:We report ChIP-Seq data for MED12 in human CD34+ cells. Med12 occupies promoter distal regions that regulate specific transcriptional programs required for the homeostasis of the hematopoietic system. 50 milion cells were used to perform ChIP from CD34+ cells with 10 ug of antibody

2016-08-25 | E-GEOD-75914 | biostudies-arrayexpress

Histone chromatin modifications in control and Med12-deficient mouse HSPCs

Project description:Using iChIP, we map H3K27Ac, H3K4me3 and H3K4me1 in small populations (HSPCs) in the presence or absence of Med12 and identify affected super-enhancers. iChIP was performed using previously published protocols (Lara-Astiaso et al, 2014 Immunogenetics. Chromatin state dynamics during blood formation - Science, 345, 6199) Examination of histone modification in mouse HSPCs with and without Med12

2016-08-25 | E-GEOD-76052 | biostudies-arrayexpress

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