Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide maps of H3K9me2 modification in wild type and jmjd1c B KO Activated B cells.

ABSTRACT: This study aims to characterize the H3K9me2 modification in wild type and jmjd1c B KO activated B cells, and find the potential mechanism of the jmjd1c B KO in activated B cells

ORGANISM(S): Mus musculus

PROVIDER: GSE195462 | GEO | 2022/07/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide maps of H3K9me2 modification in wild type and jmjd1c B KO Activated B cells.

Project description:Genome-wide maps of H3K9me2 modification in wild type and jmjd1c B KO Activated B cells.

| PRJNA800745 | ENA

Effect of loss of Jmjd1c on H3K9me2 level across the genome

Project description:Analysis of H3K9me2 level in MLL-AF9 leukemia cells upon deletion of Jmjd1c. Jmjd1c has been shown to be a H3K9me1/2 demethylase and these results provide insight into its role in MLL-Af9 leukemia

2016-06-09 | GSE75577 | GEO

RNA expression analysis upon JMJD1C depletion

Project description:The AML1-ETO fusion protein, a transcription factor generated by the t(8;21) translocation in acute myeloid leukaemia (AML), dictates a leukemic program by increasing self-renewal and inhibiting differentiation. Here we demonstrate that the histone demethylase JMJD1C functions as a co-activator for AML1-ETO and is required for its transcriptional program. JMJD1C is directly recruited by AML1-ETO to its target genes and regulates their expression by maintaining low H3K9me2 levels. Analyses in JMJD1C knockout mice also establish a JMJD1C requirement for AML1-ETO’s ability to increase proliferation. We also show a critical role for JMJD1C in the survival of multiple human AML cell lines, suggesting that it is required for leukemic programs in different AML cell types through its association with key transcription factors.

2015-11-02 | GSE63485 | GEO

RNA expression analysis upon JMJD1C depletion

Project description:The AML1-ETO fusion protein, a transcription factor generated by the t(8;21) translocation in acute myeloid leukaemia (AML), dictates a leukemic program by increasing self-renewal and inhibiting differentiation. Here we demonstrate that the histone demethylase JMJD1C functions as a co-activator for AML1-ETO and is required for its transcriptional program. JMJD1C is directly recruited by AML1-ETO to its target genes and regulates their expression by maintaining low H3K9me2 levels. Analyses in JMJD1C knockout mice also establish a JMJD1C requirement for AML1-ETOâs ability to increase proliferation. We also show a critical role for JMJD1C in the survival of multiple human AML cell lines, suggesting that it is required for leukemic programs in different AML cell types through its association with key transcription factors. Examination of RNA expression when Kasumi-1 cells are treated with control shRNA or two different JMJD1C shRNAs; in duplicate. Please note that the 'shAML1_ETO_vs_shControl.all_gene_exp.tb.txtl' was generated comparing control and shRNA treated RNA abundance-using previously published data [GSE43834; GSM1071857 and GSM1071852].

2015-11-02 | E-GEOD-63485 | biostudies-arrayexpress

Genome-wide map of JMJD1C binding in Kasumi-1 cells [ChIP-seq]

Project description:The AML1-ETO fusion protein, a transcription factor generated by the t(8;21) translocation in acute myeloid leukaemia (AML), dictates a leukemic program by increasing self-renewal and inhibiting differentiation. Here we demonstrate that the histone demethylase JMJD1C functions as a co-activator for AML1-ETO and is required for its transcriptional program. JMJD1C is directly recruited by AML1-ETO to its target genes and regulates their expression by maintaining low H3K9me2 levels. Analyses in JMJD1C knockout mice also establish a JMJD1C requirement for AML1-ETOâs ability to increase proliferation. We also show a critical role for JMJD1C in the survival of multiple human AML cell lines, suggesting that it is required for leukemic programs in different AML cell types through its association with key transcription factors. Examination of JMJD1C and LYL1 chromatin binding in Kasumi-1 cells, HL-60 cells, NB-4 cells and THP-1 cells, including ChIP-seqs of JMJD1C and LYL1, and input DNAs for Kasumi-1, HL-60, NB4.

2015-11-02 | E-GEOD-63484 | biostudies-arrayexpress

Jmjd1c

Project description:Jmjd1c

| PRJNA304620 | ENA

Next Generation Sequencing of Wild Type and jmjd1c B KO germinal center B cells and activated B cells Transcriptomes

Project description:The aim of our study is to find out the differential expression genes and differential enrichment pathways of wild type and Jmjd1c B cells specific knockout germinal center B cells and activated B cells, clarify the function of Jmjd1c in germinal center B cells and activated B cells

2022-07-08 | GSE193752 | GEO

H3K9me2 profile of tumor infiltrated Treg from the WT and the jmjd1c TregcKO mice and chromatin accessibility profile of tumor treg and spleen treg

Project description:Tumor infiltrated treg cells are considered as a crucial in the cancer immunotherapy. We used H3K9me2 CUT&RUN to analyze the differences between WT and jmjd1cTreg cko mice and clarify the important function of jmjd1c in tumor treg. We use ATACseq to analyze the difference between tumor treg and spleen treg and characterize the epigenetic characters in tumor treg.

2023-12-18 | GSE224084 | GEO

Genome-wide map of JMJD1C binding in Kasumi-1 cells [ChIP-seq]

2015-11-02 | GSE63484 | GEO

Comprehensive analysis of H3K9me2 oocytes, together with DNA methylation and expression analysis of G9a conditional KO oocytes and maternal KO preimplantation embryos

Project description:We report the first genome-wide landscape of H3K9me2 ChIP-seq profile in mouse oocytes. We also performed whole-genome bisulfite sequencing and RNA-seq analysis of G9a conditional KO oocytes and maternal KO preimplantation embryos. Our findings illuminate the functional importance of G9a in preimplantation development and, in addition, pose a question on the proposed role for H3K9me2 in protection of the maternal genome from active CG demethylation.

2019-04-02 | GSE112320 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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