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Genome-wide DNA accessibility mapping using ATAC-seq in HEK293 in vector control, PC4 knockdown and PC4 phosphorylation specific mutant and mimic

ABSTRACT: Genome-wide DNA accessibility mapping using ATAC-seq in HEK293 in vector control, PC4 knockdown and PC4 phosphorylation specific mutant and mimic

PROVIDER: PRJNA790998 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17282807_1.fastq.gz	Fastqsanger.gz
	SRR17282807_2.fastq.gz	Fastqsanger.gz
	SRR17282808_1.fastq.gz	Fastqsanger.gz
	SRR17282808_2.fastq.gz	Fastqsanger.gz
	SRR17282809_1.fastq.gz	Fastqsanger.gz

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Genome-wide DNA accessibility mapping using ATAC-seq in HEK293 in vector control, PC4 knockdown and PC4 phosphorylation specific mutant and mimic

Project description:To assess the mechanisms by which PC4 mediates chromatin compaction in cells and regulation of genome organization by its phosphorylation state, we measured the chromatin accessibility landscape using ATAC-seq of vector control 293 cells (Control/shNS), PC4 knockdown (KD/PC4 KD) and upon ectopic expression of Flag tagged PC4 (FP/PC4), Phosphomimic-PC4 (PM/PM-PC4) and phospho-mutant (MTP/MTP5) in PC4 knockdown cells.

2022-05-12 | GSE191333 | GEO

RNA-Seq analysis of MCV-miR-M1 mimic-transfected HEK293 cells

Project description:To determine transcriptomic changes in cellular targets induced by MCV-miR-M1. Briefly, HEK293 cells were transfected with either MCV-miR-M1-5p, MCV-miR-M1-3p or control mimic (Thermo Fisher Scientific) prior to RNA extraction and confirmation of MCV miRNA 5p and 3p expression via stem loop qRT-PCR. Total RNA libraries were prepared using TruSeq Stranded Total RNA Sample Prep Kit (Illumina, USA) and the TruSeq cDNA libraries were analysed via Illumina HiSeq2500 paired end 100bp.

2018-03-31 | E-MTAB-6526 | biostudies-arrayexpress

RNA-Seq analysis of MCV-miR-M1 mimic-transfected HEK293 cells

Project description:RNA-Seq analysis of MCV-miR-M1 mimic-transfected HEK293 cells

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Expression profile of HEK293 cells stably transfected with PRL-1 (PTP4A1) or empty pcDNA4 vector (control)

Project description:The multifunctional protein tyrosine phosphatase PRL-1 (Gene Symbol: PTP4A1) has been identified as an important oncogene with roles in promoting cell proliferation, survival, migration, invasion, and metastasis. However, little is currently known about the signaling pathways through which it mediates its effects. We used Affymetrix Human Genome U133 Plus 2.0 arrays to examine the global molecular changes of gene expression occurring in response to stable PRL-1 overexpression in human embryonic kidney 293 (HEK293) cells. Total RNA was extracted from triplicate cultures of HEK293 cells stably overexpressing PRL-1 (HEK293-PRL-1) and HEK293 cells stably transfected with empty pcDNA4 vector (HEK293-Vector). Samples were hybridized to Affymetrix HG U133 Plus 2.0 microarrays (1 array per sample for a total of 6 arrays). One of the arrays hybridized with a PRL-1 transfected sample was excluded after qRT-PCR demonstrated that this sample did not exhibit increased PRL-1 expression over the level of the empty vector controls. The remaining 2 HEK293-PRL-1 samples both expressed PRL-1 at least 2-fold higher than any of the 3 empty vector controls.

2013-07-30 | E-GEOD-42586 | biostudies-arrayexpress

Chromatin Protein PC4 Orchestrates B Cell Differentiation by Collaborating with IKAROS and IRF4 (RRBS)

Project description:Chromatin protein positive coactivator 4 (PC4) has multiple functions, including chromatin compaction. However, its role in immune cells is largely unknown. We show that PC4 orchestrates chromatin structure and gene expression in mature B cells. B-cell specific PC4-deficient mice showed impaired production of antibody upon antigen stimulation. The PC4 complex purified from B cells contained transcription factors IKAROS and IRF4. IKAROS protein was reduced in PC4-deficient mature B cells, resulting in de-repression of their target genes in part by diminished interactions with gene silencing components. Upon activation, IRF4 protein amount was not increased in PC4-deficient B cells, resulting in reduction of plasma cells. Importantly, IRF4 reciprocally induced PC4 expression via a super-enhancer. PC4 knockdown in human B-cell lymphoma cells reduced IKAROS protein as an anticancer drug lenalidomide. Our findings establish PC4 as a chromatin regulator of B cells and a possible therapeutic target adjoining IKAROS in B-cell malignancies.

2020-12-22 | GSE163216 | GEO

PC4 is a post-transcriptional manipulator of D-type cyclins and centromere proteins

Project description:The cell cycle is an intensively control process, in which cell-cycle proteins display a cyclical expression pattern regulated by specific transcription, translation and degradation. Cell cycle progression is initiated by highly expressed D-type cyclins (D1/2/3) to facilitate DNA synthesis, subsequently driven by mitotic proteins formation (e.g., centromere proteins) that is responsible for mitosis onset. Whether there exist master regulators to keep the cycle rapidly “running” with D-type cyclins induction, as well as maintain the cycle in a stable process by centromere proteins modulation is of particular interest yet remains unclear at present. Here our study clarifies human positive cofactor 4 (PC4) as a previously unrecognized RNA binding protein (RBP), as a post-transcriptional master regulator to orchestrate CCND1 and CENPF expression. We reveal that lack of PC4 reduces CCND1 stability whereas enhances excessive CENPF translation, results in cell cycle arrest and mitotic defects. Furthermore, PC4 RNA binding activity is strictly controlled by S17 phosphorylation and K68 ubiquitination in a cell cycle-dependent way. Lastly, we use in vivo model to verify that PC4 deficiency amplifies response of cancer cells to CDK4/6 inhibitor, and PC4 induction accelerates liver regeneration after partial hepatectomy. These results highlight that cell-cycle gene expressions are dynamically and post-transcriptionally fine-tuned, and identify PC4 as an essential cell-cycle post-transcriptional manipulator that is profoundly applied within cancer and regeneration medicine.

2024-02-03 | PXD033637 | Pride

Chromatin Protein PC4 Orchestrates B Cell Differentiation by Collaborating with IKAROS and IRF4 (Agilent microarrays)

Project description:B cell development is orchestrated by various transcription factors collaborating with chromatin remodelers that determine the genomic architecture. However, chromatin regulation in mature B cells is still poorly understood. Here, we show the critical function of positive coactivator 4 (PC4), a bona fide non-histone chromatin protein encoded by Sub1. B-cell specific Sub1-deficient mice showed the decreased number and response against antigen stimulation of mature B cells. By combining PC4 chromatin immunoprecipitation-sequencing and complex purification, we identified transcription factor IKAROS as a partner of PC4 in gene regulation. PC4 and IKAROS cooperated to promote heterochromatin formation of their target gene loci and thereby established B cell identity. Importantly, PC4 stabilized IKAROS protein in mature B cells and inhibited IKAROS degradation by the anti-cancer drug lenalidomide in human B-cell lymphoma cells. These findings establish PC4 as not only a chromatin regulator of B cells but also a new therapeutic target in B-cell malignancies.

2020-12-22 | GSE145952 | GEO

Chromatin Protein PC4 Orchestrates B Cell Differentiation by Collaborating with IKAROS and IRF4 (ChIP-seq)

2020-12-22 | GSE145951 | GEO

PC4 is a post-transcriptional manipulator of D-type cyclins and centromere proteins (eCLIP-Seq).

Project description:To investigate the binding site in which PC4 protein association with its target RNAs. eCLIP-seq was performed to profile PC4-binding RNA targets in Huh7 cells.

2024-02-12 | GSE202400 | GEO

Importance of Transcriptional coactivator PC4 in p53-dependent Genotoxic Stress Response

Project description:In order to get an idea of involvement of PC4 in regulation of p53-dependent gene expression, we carried out global gene expression profiling upon treatment with R6-NLS-p53(380–386-3Ac). R6-NLS-p53(380–386-3Ac) is a small peptide of 20 residues derived from p53 C-terminal domain. This peptide can successfully block the cellular p53-PC4 interactions. Lung cancer line A549 which contain both wild type p53 and PC4 were used for this study. The cells were treated with 25µM R6-NLS-p53(380–386-3Ac) for two different time points (12 h and 24 h) and the gene expression profile was analyzed by microarray analysis.

2019-06-21 | GSE116020 | GEO

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