Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

H3K4me2 ChIP-seq upon GSK inhibiton

ABSTRACT: H3K4me2 ChIP-seq upon GSK inhibiton

PROVIDER: PRJNA543247 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9070080.fastq.gz	Fastqsanger.gz
	SRR9070081.fastq.gz	Fastqsanger.gz
	SRR9070082.fastq.gz	Fastqsanger.gz
	SRR9070083.fastq.gz	Fastqsanger.gz
	SRR9070084.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

H3K4me2 ChIP-seq upon GSK inhibiton

Project description:We show in prostate cancer cells that LSD1 co-localizes with FOXA1 and active enhancer markers (H3K4me2), and that LSD1 inhibition globally disrupts FOXA1 chromatin binding.

2019-09-29 | GSE131321 | GEO

CUT & RUN analysis of H3K4me2 mark upon LSD1 inhibition

Project description:CUT & RUN analysis of H3K4me2 mark upon LSD1 inhibition

| PRJNA985560 | ENA

Chip-chip of Set3, of PolII, and of H3K4me2 from budding yeast cells

Project description:Chromatin immunoprecipitation of Set3, of PolII, and of H3K4me2, respectively, applied with tilling array chip (ChIP on chip of Set3, of PolII, and of H3K4me2, respectively) analysis demonstrated that a compared genomic occupancy of Set3, of PolII, and of H3K4me2 in Saccharomyces cerevisiae wild type cells compared anong those in Hst1 deleted, Hos2 deleted and Hst2 & Hos2 double deleted cells

2020-12-31 | GSE143665 | GEO

Chip-chip of Snt1, of PolII, and of H3K4me2 from budding yeast cells

Project description:Chromatin immunoprecipitation of Snt1, of PolII, and of H3K4me2, respectively, applied with tilling array chip (ChIP on chip of Snt1, of PolII, and of H3K4me2, respectively) analysis demonstrated that a compared genomic occupancy of Snt1, of PolII, and of H3K4me2 in Saccharomyces cerevisiae wild type cells compared anong those in Hst1 deleted, Hos2 deleted and Hst2 & Hos2 double deleted cells

2020-12-31 | GSE143667 | GEO

Gene expression in astrocytes upon sustained GSK-3 inhibition by small molecule

Project description:In order to identify molecular targets that mediates the stimulation of astrocyte's migration upon sustained specific inhibition of GSK-3, we have employed whole genome microarray expression profiling. Murine cortical-striatal astrocytes grown in primary culture were treated in vitro for 48 h with either 1 micromolar Ro3303544, or control medium (final equivalent concentration of DMSO), or washed-out for 48h in control medium after an initial 48h treatment with 1 micromolar Ro3303544. The three different conditions: Ctrl, Ro and wash-out (each in duplicate) were compared.

2011-08-31 | E-GEOD-25770 | biostudies-arrayexpress

CUT & RUN analysis of H3K4me2 mark upon LSD1 inhibition

Project description:Lysine-specific demethylase 1 (LSD1) is a histone demethylase that promotes stemness and cancer cell survival, including in prostate cancer. LSD1 has been shown to perfrom catalytic independent function sto promote prostate cancer survival. Here, we tested the levels of LSD1's canonical target H3K4me2 upon LSD1 inhibition with SP2509 across the genome using CUT and RUN analysis.

2023-08-30 | GSE235211 | GEO

GSK-3A and GSK-3B knockdown in AML cell lines

Project description:Gene expression data from AML cell lines, MOLM-14, U937, THP-1 and HL-60, that were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), or two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6). Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long-term survival of patients with AML has changed little over the past decade, necessitating the identification and validation of new AML targets. Integration of genomic approaches with small-molecule and genetic-based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. Here, we identified a role for glycogen synthase kinase 3A (GSK-3A) in AML by performing two independent small-molecule library screens and an shRNA screen for perturbations that induced a differentiation expression signature in AML cells. GSK-3 is a serine-threonine kinase involved in diverse cellular processes including differentiation, signal transduction, cell cycle regulation, and proliferation. We demonstrated that specific loss of GSK-3A induced differentiation in AML by multiple measurements, including induction of gene expression signatures, morphological changes, and cell surface markers consistent with myeloid maturation. GSK-3AM-bM-^@M-^Sspecific suppression also led to impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in methylcellulose, and anti-AML activity in vivo. Although the role of GSK-3B has been well studied in cancer development, these studies support a role for GSK-3A in AML. The AML cell lines, MOLM-14, U937, THP-1 and HL-60, were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), and two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6).

2012-02-27 | E-GEOD-35200 | biostudies-arrayexpress

h3k4me2-Establishing a reference epigenome in arabidopsis seedlings

Project description:gfe_epigenome - h3k4me2 - Epigenomic mapping - H3K4me2 ChIP-chip

2011-04-19 | GSE24648 | GEO

Genome-wide ChIP-Seq from GSK-J4 or siKDM6B-treated lung adenocarcinoma cell line A549

Project description:Purpose: The goals of our study were to identify downstream pathway regulated by GSK-J4 in lung adenocarcinoma Methods: Chromatin isolated from GSK-J4- or siKDM6B-treated lung adenocarcinoma with proper controls was used to generate ChIP-Seq libraries

2021-08-08 | GSE133967 | GEO

AR ChIP-seq with DHT induction and GSK treatment

Project description:AR ChIP-seq with DHT induction and GSK treatment

| PRJNA470713 | ENA