Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

40 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Role of the histone demethylase KDM2B in hematopoietic homeostasis and malignancies

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Alexandros Tzatsos

PROVIDER: E-GEOD-70729 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Histone demethylase KDM2B regulates lineage commitment in normal and malignant hematopoiesis.

Andricovich Jaclyn J Kai Yan Y Peng Weiqun W Foudi Adlen A Tzatsos Alexandros A

The Journal of clinical investigation 20160125 3

The development of the hematopoietic system is a dynamic process that is controlled by the interplay between transcriptional and epigenetic networks to determine cellular identity. These networks are critical for lineage specification and are frequently dysregulated in leukemias. Here, we identified histone demethylase KDM2B as a critical regulator of definitive hematopoiesis and lineage commitment of murine hematopoietic stem and progenitor cells (HSPCs). RNA sequencing of Kdm2b-null HSPCs and ...[more]

PMID: 26808549

Similar Datasets

Role of the histone demethylase KDM2B in hematopoietic homeostasis and malignancies [human cell line gene expression]

Project description:Development of the hematopoietic system is dynamically controlled by the interplay of transcriptional and epigenetic networks to determine cellular identity. Those networks are critical for homeostasis and frequently dysregulated in leukemias. We identified histone demethylase Kdm2b as a critical regulator of definitive hematopoiesis and lineage specification of hematopoietic stem and progenitor cells (HSPCs). RNA sequencing in murine HSPCs and genome-wide chromatin immunoprecipitation studies in human leukemias revealed that Kdm2b regulates differentiation, lineage choice, cytokine signaling, and quiescence. Identify the KDM2B dependent transcriptome in human leukemia cell lines by using the GeneChipÂ® PrimeViewâ¢ Human Gene Expression Array

2016-02-22 | E-GEOD-74959 | biostudies-arrayexpress

Role of the histone demethylase KDM2B in hematopoietic homeostasis and malignancies [Kras background mouse gene expression]

Project description:Development of the hematopoietic system is dynamically controlled by the interplay of transcriptional and epigenetic networks to determine cellular identity. Those networks are critical for homeostasis and frequently dysregulated in leukemias. We identified histone demethylase Kdm2b as a critical regulator of definitive hematopoiesis and lineage specification of hematopoietic stem and progenitor cells (HSPCs). RNA sequencing in murine HSPCs and genome-wide chromatin immunoprecipitation studies in human leukemias revealed that Kdm2b regulates differentiation, lineage choice, cytokine signaling, and quiescence. Comparison of gene expression in wild-type and knockout HSPCs We analyzed lineage depleted cells isolated from bone marrow from mice that express oncogenic Kras in the context of knockout and overexpression of Kdm2b in Affymetrxi GeneChipÂ® Mouse Gene 2.0 ST Array

2016-02-22 | E-GEOD-74960 | biostudies-arrayexpress

Role of the histone demethylase KDM2B in hematopoietic homeostasis and malignancies [RNA-seq]

Project description:Development of the hematopoietic system is dynamically controlled by the interplay of transcriptional and epigenetic networks to determine cellular identity. Those networks are critical for homeostasis and frequently dysregulated in leukemias. We identified histone demethylase Kdm2b as a critical regulator of definitive hematopoiesis and lineage specification of hematopoietic stem and progenitor cells (HSPCs). RNA sequencing in murine HSPCs and genome-wide chromatin immunoprecipitation studies in human leukemias revealed that Kdm2b regulates differentiation, lineage choice, cytokine signaling, and quiescence. Comparison of gene expression in wild-type and knockout HSPCs

2016-02-22 | E-GEOD-70728 | biostudies-arrayexpress

Proteomics analysis of HepG2 after administration of dehydroabietic acid

Project description:Proteomics identification of the HepG2 test group after administration of dehydroabietic acid was implemented to disclose the influencing mechanism of dehydroabietic acid on HepG2.

2022-11-22 | PXD036015 | Pride

ZMYND11-MBTD1 induces leukemogenesis through hijacking NuA4/TIP60 acetyltransferase complex and a PWWP-mediated chromatin association mechanism

Project description:Recurring chromosomal translocation t(10;17)(p15;q21) present in a subset of human acute myeloid leukemia (AML) patients creates an aberrant fusion gene termed ZMYND11-MBTD1 (ZM); however, its function remains undetermined. Here, we show that ZM confers primary murine hematopoietic stem/progenitor cells indefinite self-renewal capability ex vivo and causes AML in vivo. Genomics profilings reveal that ZM directly binds to and maintains high expression of pro-leukemic genes including Hoxa, Meis1, Myb, Myc and Sox4. Mechanistically, ZM recruits NuA4/Tip60 histone acetyltransferase complex to cis-regulatory elements, sustaining an active chromatin state enriched in histone acetylation and devoid of repressive histone marks. Systematic mutagenesis of ZM demonstrates essential requirements of Tip60 interaction and an H3K36me3-binding PWWP domain for oncogenesis. Inhibitor of histone acetylation-‘reading’ bromodomain proteins, which act downstream of ZM, is efficacious in treating ZM-induced AML. Collectively, this study demonstrates AML-causing effects of ZM, examines its gene-regulatory roles, and reports an attractive mechanism-guided therapeutic strategy.

2021-01-21 | PXD023702 | Pride

RNA-seq transcriptional profiling in human primary fetal and adult CD34+ hematopoietic stem/progenitor cells (HSPCs) erythroid progenitor cells (ProEs)

Project description:Advances in sequencing-based genomic profiling present a new challenge of explaining how changes in DNA/RNA are translated into proteins linking genotypes to phenotypes. The developing erythroid cells require highly coordinated gene expression and metabolism, and serve as a unique model in dissecting regulatory events in development and disease. Here we compare the proteomic and transcriptomic changes in human hematopoietic stem/progenitor cells and lineage-committed erythroid progenitors, and uncover pathways related to mitochondrial biogenesis enhanced through post-transcriptional regulation. Two principal mitochondrial factors TFAM and PHB2 are tightly regulated at the protein level and indispensable for mitochondria and erythropoiesis. mTORC1 signaling is progressively enhanced to promote translation of mitochondrial proteins during erythroid specification. Genetic and pharmacological perturbation of mTORC1 or mitochondria impairs erythropoiesis. Our studies suggest a new mechanism for regulation of mitochondrial biogenesis through mTORC1-mediated protein translation, and may have direct relevance to the hematological defects associated with mitochondrial diseases and aging. Transcriptional profiling in human primary fetal and adult CD34+ hematopoietic stem/progenitor cells (HSPCs) erythroid progenitor cells (ProEs) by RNA-seq analysis.

2017-05-15 | E-GEOD-74053 | biostudies-arrayexpress

RNA-seq of CN, CN/AML, and CN/AML BAALC KO iPSCs-derived HSPCs

Project description:Severe congenital neutropenia (CN) is a pre-leukemia syndrome that, in the majority of patients, is caused by heterogeneous ELANE mutations encoding neutrophil elastase (NE). To study leukemogenesis associated with CN we generated CN and CN/AML patient-specific induced pluripotent stem cells (iPSCs). Additional mutations in leukemia-relevant genes, CSF3R and RUNX1, were introduced using CRISPR/Cas9 gene-editing. Consequently, we performed in vitro embryoid body (EB)-based hematopoietic and myeloid differentiation of generated iPSC lines. On day 14-17 of EB-based differentiation, iPSC-derived CD45+CD34+ cells were harvested and mRNA was isolated using RNeasy Mini- or Micro Kit (Qiagen). Sequencing libraries were prepared using the TruSeq RNA Sample Prep Kit (Illumina). Poly (A) selected single-read and pair-read sequencing libraries were sequenced on the Illumina platform in order to compare the transcriptomes of CN and CN/AML iPSCs-derived HSPCs from 2 CN/AML patients. Next, we identified that BAALC knockout resulted in a dramatic induction of granulocytic differentiation and a significant reduction in proliferation of CN/AML iPSC-derived HSPCs. To identify BAALC-dependent leukemia-associated gene expression, we compared the transcriptomes of CN/AML iPSCs before and after BAALC KO using a similar approach described above for CN and CN/AML iPSCs-derived HSPCs.

2021-03-08 | E-MTAB-10162 | biostudies-arrayexpress

Jarid2 regulates hematopoietic stem cell function by acting with Polycomb Repressive Complex 2

Project description:Polycomb Repressive Complex 2 (PRC2) has been shown to play a key role in hematopoietic stem and progenitor cell (HSPC) function. Analyses of mouse mutants harboring deletions of core components have implicated PRC2 in fine-tuning multiple pathways that instruct HSPC behavior, yet how PRC2 is targeted to specific genomic loci within HSPCs remains unknown. Here we use shRNA-mediated knockdown to survey the function of known PRC2 accessory factors in HSPCs by testing the competitive reconstitution capacity of transduced murine fetal liver cells. We find that similar to the phenotype observed upon depletion of core subunit Suz12, depleting Jarid2 enhances the competitive transplantation capacity of both fetal and adult, mouse and human HSPCs. Gene expression profiling revealed common Suz12 and Jarid2 target genes that are enriched for the H3K27me3 mark established by PRC2. These data implicate Jarid2 as an important component of PRC2 that has a central role in coordinating HSPC function. RNA-seq of jarid knockdown, suz knockdown and control from HSPC in 16 week old mice.

2015-04-02 | E-GEOD-60808 | biostudies-arrayexpress

KDM2B links the Polycomb Repressive Complex 1 (PRC1) to recognition of CpG islands

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2012-12-26 | E-GEOD-41267 | biostudies-arrayexpress

Reprogramming of bone marrow myeloid progenitor cells in patients with severe coronary atherosclerosis

Project description:Innate immune cells importantly contribute to the pathphysiology of atherosclerotic cardiovascular disease CVD. Previous studies show that isolated innate immune cells from patients with atherosclerotic CVD have an activated phenotype. To understand the origin of this immune cell activation, we performed bone marrow aspiration in 10 male patients with severe coronary artery disease (based on coronary CT angiography) and 10 control subjects in whom coronary atherosclerosis was excluded. After flow sorting of HSCs, MPPs, and GMPs, we performed RNAseq.

2020-11-08 | E-MTAB-9399 | biostudies-arrayexpress

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