Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide map of H3K27me3 before and after AKBA treatment in HaCaT cells

ABSTRACT: Genome-wide map of H3K27me3 before and after AKBA treatment in HaCaT cells

PROVIDER: PRJNA439422 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6874053_1.fastq.gz	Fastqsanger.gz
	SRR6874053_2.fastq.gz	Fastqsanger.gz
	SRR6874054_1.fastq.gz	Fastqsanger.gz
	SRR6874054_2.fastq.gz	Fastqsanger.gz
	SRR6874055_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Genome-wide map of H3K27me3 before and after AKBA treatment in HaCaT cells

Project description:The goal of this study was to compare the distribution of H3K4me3 before and after AKBA treatment to understand how small molecule AKBA affects the epigenetic state. To do this we performed ChIP-seq with an H3K27me3 antibody.

2018-03-22 | GSE112142 | GEO

transcriptome-wide map of NCSTN-KD and NC Hacat cells

Project description:transcriptome-wide map of NCSTN-KD and NC Hacat cells

| PRJNA862925 | ENA

transcriptome-wide map of NCSTN-KD and NC Hacat cells

Project description:Acne inversa (AI) is an inflammatory skin disease associated with the nicastrin (NCSTN) mutations. Family history with autosomal dominant inheritance has heen reported in AI patients and are associated with mutations in the γ-secretase subunit, nicastrin (NCSTN), presenilin enhancer 2 (PSENEN), and presenilin-1 (PSEN1). Among them, NCSTN gene has the highest mutation rate. To detect the impact of NCSTN deficiency on AI keratinocytes. Here, using the short hairpin RNA (shRNA)-mediated gene knockdown and RNA sequencing technology, we explored the differentially expressed genes regulated by NCSTN deficiency in HaCaT cells.

2023-12-31 | GSE209911 | GEO

Genome wide map of H3K27me3 histone mark remeains unaltered after silecing of lncRNA SCIRT

Project description:We generated genome wide map of H3K27me3 histone mark in mammospheres where we silenced lncRNA SCIRT, PRC2 member EZH2. We discovered that upon silencing of lncRNA SCIRT and EZH2, the distribution of this histone mark does not change. This indicates that lncRNA SCIRT is important for EZH2 function that is independant of its activity as a histone methyltranspherase.

2021-02-23 | GSE136186 | GEO

Human keratinocytes HaCaT LC-MSMS_SDS exposure

Project description:We employed human HaCaT cells as a model system to identify cellular proteins that accompany SDS-induced toxicity based on a proteomic approach. HaCaT human keratinocyte cell line were treated with a non-cytotoxic dose of SDS (25 µg/ml, as determined by the MTT assay and microscopically examination) for 48 h. The altered abundance of proteins from HaCaT keratinocytes exposed to SDS was analyzed by LC-MS/MS approach and quantified using Progenesis LC software. The abundance of 217 proteins (which were identified by multiple peptides, ≥ 2) was altered in keratinocytes exposed to SDS; in which 131 proteins had increased abundance while 86 proteins was down regulated. The Pathview map of 131 up-regulated proteins was built and enhancement of glycolysis/gluconeogenesis was found.

2017-11-03 | PXD007789 | Pride

Genome wide map of H3K27me3 histone mark remeains unaltered after silecing of lncRNA SCIRT

Project description:Genome wide map of H3K27me3 histone mark remeains unaltered after silecing of lncRNA SCIRT

| PRJNA561539 | ENA

Gene expression profiling of cidofovir treatment and resistance inHeLa, HaCaT, and PHK cells

Project description:Cidofovir is an acyclic nucleoside phosphonate with strong antiviral activity against a broad spectrum of DNA viruses. Although it has previously been shown that cidofovir exerts an antiproliferative effect on HPV positive cells by the induction of apoptosis, the exact mechanism of action remains to be unraveled. In order to study the activity of cidofovir against HPV, gene expression profiling was performed in cidofovir-treated and cidofovir-resistant HeLa, HaCaT, and PHK cells by means of microarrays (HG-U133 Plus 2, Affymetrix). Controls (untreated HeLa, HaCaT, and PHK wild-type cells): 72h of growth. Cidofovir treated (50 M-BM-5g/ml) HeLa, HaCaT, and PHK cells: 72h of growth. Cidofovir resistant cells (HeLa #52 and HaCaT #51): 72h of growth. All samples were performed in triplicates.

2013-07-03 | E-GEOD-39293 | biostudies-arrayexpress

Protein dataset of immortalized HaCaT cells p53 knock down HaCaT keratinocytes

Project description:The p53 protein is encoded by TP53 gene and plays the key role in significant number of cellular processes including proliferation, apoptosis and regulation of many stress response pathways. P53 acts like a direct transcription activator of numerous genes regulating cell cycle arrest, DNA repair, growth inhibition and many others (Mollereau and Ma, 2014). The canonical biological function of p53 is maintaining genome integrity via elimination of damaged or exposed to genotoxic stress cells. Immortalized HaCaT cells are widely used for keratinocyte research, since they maintain stable keratinocyte phenotype, have nearly unlimited proliferative potential, do not require specific growth and differentiation factors (Colombo et al., 2017). Also, HaCaT cells produce typical differentiation markers such as cytokeratins K14 and K10, involucrin (Colombo et al., 2017) and respond to keratinocyte differentiation stimuli. Taking together, HaCaT cells have similar to normal human keratinocytes (NHK) properties, however, as many of spontaneously immortalized cell lines HaCaT cells bear two mutant p53 alleles - R282Q and H179Y (Lehman et al., 1993). Mutp53 in HaCaT has an increased affinity to other p53 family members (p63, p73), which significantly expands p53 properties. Moreover, mutp53 indirectly affects specific target genes via protein-protein interactions with other transcription factors (NF-Y, E2F1, NF-KB) or by tethering p63 to new promotor locations. For more detailed investigation of mutp53 impact on various processes in HaCaT cells we performed a shRNA mediated knockdown of mutp53. For generation of stable TP53 knockdown we employed plasmid vector pLKO-p53-shRNA-941 (Addgene # #25637) followed by puromycin selection of transduced cells. Here we present proteomic dataset obtained from wild type HaCaT cells and p53 knock down HaCaT keratinocytes.

2022-04-28 | PXD033538 | Pride

Study of transcriptional effects of monosodium urate crystal (MSU) on HaCaT keratinocyte cell line.

Project description:Aim of the study was to characterize at a molecular level (changes in transcriptomes) the effect of monosodium urate crystal (MSU) on HaCaT keratinocyte cell line. This was adressed by using a culture model. The HaCaT cell line (human keratinocytes) was stimulated by MSU (1mg/mL) vs control for 12 hrs. By using genome-wide expression profiling, we identified deregulation of functionally relevant gene networks. HaCaT were obtained from Cell Lines Service (Eppelheim, Germany) and grown in DMEM medium (PAN biotech, Aidenbach, Germany) supplemented with 10% FBS (Life Technology, Grand Island, NY, USA), L-glutamine and non-essential amino acid. Before the treatment HaCaT cells were cultured in serum-free medium for 12hrs. HaCaT were treated with MSU (1mg/ml) vs DMEM control for 12hrs then submitted to RNA extration and gene expression profiling. Triplicate experiments were performed: HaCaT control (n=3), MSU-treated (n=3).

2015-10-29 | E-GEOD-65931 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of HaCaT and OSM-treated HaCaT Transcriptomes

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare transcriptome profiling (RNA-seq) between HaCaT cell and OSM-treated HaCaT cells Methods: mRNA profiles of HaCaT cells and OSM-treated HaCaT cells were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks.

2021-03-18 | GSE150994 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data