Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of KAT6B signature on KAT6B deficient SCLC cell Lines

ABSTRACT: To develop our gene expression experiment, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentially regulated by the transcriptional coactivator KAT6B. Expression of KAT6B gene was downregulated in two human SCLC cell lines using two different short hairpin RNAs. RNAs from these modified cell lines were hybridized in Agilent platform.

ORGANISM(S): Homo sapiens

PROVIDER: GSE59136 | GEO | 2015/10/07

SECONDARY ACCESSION(S): PRJNA254479

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

KAT6B gene deletion in small cell lung cancer

Project description:Copy number analysis of KAT6B gene deletion in small cell lung cancer cell lines

2015-10-07 | GSE62773 | GEO

Homo sapiens

Project description:Identification of KAT6B signature on KAT6B deficient SCLC cell Lines

| PRJNA254479 | ENA

RNA-seq Analysis of mouse SCLC cell lines with or without Kdm1a knock-out

Project description:Purpose: Histone demethylase Kdm1a affected mouse SCLC progression through many down-stream factors or pathways. RNA-seq of mouse SCLC cell lines with or without Kdm1a knock-out was used to find the most enriched pathways in Kdm1a knock-out cells Methods: Total mRNA profiles of control (Crispr-V2) or Kdm1a knock-out mouse SCLC cell lines (Kdm1a-sg1, Kdm1a-sg2) were generated by deep sequencing, using Illumina Hiseq platform and 125 bp/150 bp paired-end reads. Index of the reference genome was built using Bowtie v2.2.3 and paired-end clean reads were aligned to the reference genome using TopHat v2.0.12. qRT–PCR validation was performed using TaqMan and SYBR Green assays Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm9). Commonly differential expression after Kdm1a knock-out with two different single guide RNAs to control mouse SCLC cells were selected with a fold change ≥1.5. Conclusions: Our data showed four Rest related pathways, including negative cell proliferation, negative cell differentiation, positive regulation of programmed cell death enriched, in commonly up-regulated genes after Kdm1a knock-out with twe different single guide RNAs. Meanwhile, the commonly down-regulated genes were mostly enriched in neron related pathways. These result illustrated the Kdm1a depletion inhibited mouse SCLC progression, defected its neuroendocrine phenotype through the up-regulation of Rest.

2022-01-20 | GSE125448 | GEO

Identification of MAX signature on MAX deficient SCLC cell lines

Project description:To development our gene expression approach, we have employed whole genome microarray expression profiling as a discovery platform to identify genes potentialy regulated by the transcription factor MAX.Human SCLC cell lines waere analyzed for mutations at the MAX locus. Those cell lines that were found mutated in MAX and showed no MAX protein expression were used as a models to restore the expression of MAX transcription factor, and Identify MAX signature on Human SCLC. Human SCLC cell lines were hybridyzed in the following manner according for different conditions (Mock -Ø, MAX, shBRG1, MAX-shBRG1): 3 different biological samples for Mock, 3 different biological samples for MAX, 3 different samples for shBRG1 and 3 replicates of the same sample for MAX-shBRG1.

2013-12-28 | E-GEOD-48559 | biostudies-arrayexpress

Identification of MAX signature on MAX deficient SCLC cell lines

2013-12-28 | GSE48559 | GEO

PM01183 on SCLC cell lines

Project description:PM01183 on SCLC cell lines

| PRJNA742056 | ENA

The histone acetyltransferase KAT6B is required for haematopoietic stem cell development and function

Project description:The histone lysine acetyltransferase KAT6B (MYST4, MORF, QKF) is the target of recurrent chromosomal translocations causing haematological malignancies with poor prognosis. Using Kat6b germline deletion and overexpression in mice, we determined the role of KAT6B in the haematopoietic system. We found that KAT6B sustained the fetal haematopoietic stem cell pool but did not affect viability or differentiation. KAT6B was essential for normal levels of histone H3 lysine 9 (H3K9) acetylation but not for a previously proposed target, H3K23. Compound heterozygosity of Kat6b and the closely related gene, Kat6a, abolished haematopoietic reconstitution after transplantation. KAT6B and KAT6A cooperatively promoted transcription of genes regulating haematopoiesis, including the Hoxa cluster, Pbx1, Meis1, Gata family, Erg and Flt3. In conclusion, we identified the haematopoietic processes requiring Kat6b and showed that KAT6B and KAT6A synergistically promoted HSC development, function and transcription. Our findings are pertinent to current clinical trials testing KAT6A/B inhibitors as cancer therapeutics.

2024-02-25 | GSE256039 | GEO

RNA sequencing of cortical neurons from Kat6b deficient mouse foetuses

Project description:The RNA sequencing data are part of a study reporting and investigating a mouse model of the Say-Barber-Biesecker-Young-Simpson (SBBYS) syndrome (OMIM:603736) and demonstrating proof-of-principle efficacy of postnatal treatment with sodium valproate (VPA) or acetyl-carnitine (ALCAR). The KAT6B gene encodes a histone lysine acetyltransferase. The RNA sequencing experiments identified genes that are differentially expressed between Vehicle treated Kat6b+/– and Kat6b+/+ cortical neurons and the subset genes that are restored to normal expression after treatment with ALCAR or VPA. Cortical neurons were isolated from four Kat6b+/– and four Kat6b+/+ E16.5 mouse cerebral cortex. Cells from each cortical neuron isolate were cultured with 1 mM ALCAR, 1 mM VPA or untreated medium (Vehicle) for 4 days.

2024-01-28 | GSE249964 | GEO

Effects of loss and gain of KAT6B on gene expression in the developing cerebral cortex [Myst4_RNAseq]

Project description:High histone acetylation is associated with high transcriptional activity. The lysine acetyltransferase KAT6B is known to be required for histone acetylation and KAT6B is essential for normal brain development. In this study we examined the effects of loss and gain of KAT6B on gene expression in the developing cerebral cortex. We isolated RNA from the dorsal telencephalon of embryonic day 12.5 embryos, which is the primordium of the cerebral cortex, and from the E15.5 foetal cortex of mouse embryos and foetuses that lacked KAT6B or overexpressed KAT6B. Genes required for brain development and neuronal differentiation were downregulated in Kat6b null tissues and upregulated in Kat6b transgenic overexpressing tissue.

2024-11-06 | GSE280784 | GEO

Effects of loss and gain of the histone acetyltransferase KAT6B on DNA accessibility (ATAC-seq)

Project description:Heterozygous mutations in the histone acetyltransferase gene KAT6B (MYST4/MORF/QKF) cause cognitive disorders. Congruently, KAT6B is required for brain development, neural stem cell self-renewal and neuronal differentiation in mice. Despite the clear requirement for KAT6B in brain development, its molecular roles remain unexplored. Here we use ATAC sequencing to determine the effects of loss or gain of KAT6B on DNA accessiblity.

2024-11-06 | GSE267675 | 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