Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [RNA-seq]

ABSTRACT: Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [RNA-seq]

PROVIDER: PRJNA412206 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6076940.fastq.gz	Fastqsanger.gz
	SRR6076941.fastq.gz	Fastqsanger.gz
	SRR6076938.fastq.gz	Fastqsanger.gz
	SRR6076939.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Loss of KDM4B exacerbates bone-fat imbalance and mesenchymal stromal cell exhaustion in skeletal aging

Project description:Loss of KDM4B exacerbates bone-fat imbalance and mesenchymal stromal cell exhaustion in skeletal aging

| PRJNA412178 | ENA

Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [ChIP-seq]

Project description:Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [ChIP-seq]

| PRJNA412202 | ENA

Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [ChIP-seq]

Project description:Mesenchymal stem/stromal cells (MSCs) are multipotent progenitor cells with multilineage differentiation potentials. We previously reported histone demethylases KDM4B promoted osteogenesis and inhibited adipogenesis of human MSCs. To identify genome-wide enrichments of KDM4B and the changes in H3K9me3 marks when loss of KDM4B, Primary MSCs were isolated from Prx1Cre; Kdm4bf/f mice and control mice. ChIP-seq assay was performed using KDM4B, H3K9me3 and H3 antibody, respectively.

2021-02-10 | GSE104257 | GEO

Loss of KDM4B exacerbates bone-fat imbalance and mesenchymal stromal cell exhaustion in skeletal aging

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-10 | GSE104259 | GEO

Loss of KDM4B Exacerbates Bone-Fat Imbalance and Mesenchymal Stem Cell Exhaustion in Skeletal Aging [RNA-seq]

Project description:Primary mMSCs were cultured in control medium (Con), containing DMEM and 15% FBS, or were subjeucted to osteogenic induction (OI) for 2 days. RNA was isolated using RNeasy Mini Kit (Qiagen, Cat#74104) from three biological replicates of primary MSCs from Prx1Cre;Kdm4bf/f mice and control mice. Total RNA was then purified with Dynabeads™ mRNA Purification Kit (Invitrogen, Cat#61006). RNA-seq libraries were constructed using Stranded RNA-Seq Library Preparation Kit (Kapa Biosystems, Cat#KK8400), and sequenced using an illumina HiSeq 3000 sequencer at the Technology Center for Genomics & Bioinformatics (TCGB) core at UCLA.

2021-02-10 | GSE104258 | GEO

ChIP-seq of Danio rerio wild type and kdm4b mutant embryos to investigate kdm4b signaling

Project description:chromatin immunoprecipitation sequencing (ChIP-seq) was performed to identify the targeted genes of kdm4b

2024-07-01 | E-MTAB-13114 | biostudies-arrayexpress

Expression analysis of blastocysts in Kdm4b-PEs

Project description:To identify the genes that are controled by H3K9me3 modification in PEs, we conducted transcriptome analysis using Egfp-, Kdm4b-PEs, and IVF embryos at blastocyst stages. Kdm4b or Egfp mRNA injected oocytes were parthenogenetically activated. IVF embryos were generated according to standard protcol. All embryos were cultured in KSOM medium for 120 hours after activation or sperm insemination. Five blastocysts per one biological replicate were pooled and analyzed.

2014-11-15 | E-GEOD-53662 | biostudies-arrayexpress

Transcriptomic analysis of KDM4B-mediated genes in AGS cells

Project description:KDM4B, an important epigenetic regulator of cell proliferation, metastasis and genome stability, is often overexpressed in gastric cancer. Notably, elevated expression of KDM4B is associated with a poor clinical outcome. A global transcriptomic analysis between KDM4B control and KDM4B-knockdown AGS cells without or with Helicobacter pylori challenge reveals differentially expressed genes involved in response to virus, multi-organism process, and response to stimulus, suggesting KDM4B as an inducible epigenetic factor under H. pylori challenge.

2019-02-05 | GSE107703 | GEO

KDM4B- and KDM6B-regulated genes in human mesenchymal stem cell osteogenic differentiation

Project description:To investigate how histone demethylases KDM4B and KDM6B may be involved in osteogenic commitment of mesenchymal stem cells (MSCs), we performed gene expression profiling and comparison on control, KDM4B- and KDM6B-knockdown MSCs at different stages of osteogenic differentiation. Human MSCs infected with scramble shRNAs, shRNAs against KDM4B or KDM6B are treated with BMP4/7 for 0, 4 and 24hrs. Total RNA were extracted from these 9 samples.

2012-07-31 | E-GEOD-36970 | biostudies-arrayexpress

Histone demethylase KDM4B promotes DNA damage by activating long interspersed nuclear element-1

Project description:We assess whole-genome H3K9me3 distribution in cancer cells and find that H3K9me3 is largely enriched in long interspersed nuclear element-1 (LINE-1). A significant proportion of KDM4B-dependent H3K9me3 was located in evolutionarily young LINE-1 elements, which likely retain retrotransposition activity. Ectopic expression of KDM4B promoted LINE-1 expression, while depletion of KDM4B reduced it. Furthermore, KDM4B overexpression enhanced LINE-1 retrotransposition efficacy, copy number, and associated DNA damage, presumably via the histone demethylase activity of KDM4B. Breast cancer cell lines expressing high levels of KDM4B also exhibited increased LINE-1 expression and copy number compared with other cell lines. Pharmacological inhibition of KDM4B significantly reduced LINE-1 expression and DNA damage in breast cancer cells with excessive KDM4B. Our study not only identifies KDM4B as a novel regulator of LINE-1, but it also suggests an unexpected oncogenic role for KDM4B overexpression in tumorigenesis, providing clues for the development of new cancer prevention strategies and therapies.

2018-10-24 | GSE121642 | 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