Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of ASXL2 shRNA KD in SKNO-1 cells

ABSTRACT: The goals of this study are to compare transcriptome profiling (RNA-seq) of Asxl2 knockdowned SKNO-1 cells to control SKNO-1 cells. We found substantial number of genes are differentially expressed in Asxl2 knockdowned cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE84358 | GEO | 2017/06/26

SECONDARY ACCESSION(S): PRJNA328992

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq of Asxl2 KO LSK cells

Project description:The goals of this study are to compare transcriptome profiling (RNA-seq) of Asxl2 KO LSK cells to that of Asxl2 wild-type cells. We found substantial number of genes are differentially expressed in Asxl2 KO cells.

2017-06-26 | GSE84357 | GEO

ChIP-seq of ASXL2 in SKNO1 cells

Project description:The goals of this study are to identify ASXL2 binding sites in SKNO1 cells

2017-06-26 | GSE84363 | GEO

ChIP-seq of H3K27Ac in SKNO1 cells after knockdown of ASXL2

Project description:The goals of this study are to identify the changes of H3K27Ac in SKNO1 cells after knockdown of ASXL2

2017-06-26 | GSE93164 | GEO

ChIP-seq of H3K27me3 in SKNO1 cells after knockdown of ASXL2

Project description:The goals of this study are to identify the changes of H3K27me3 in SKNO1 cells after knockdown of ASXL2

2017-06-26 | GSE84362 | GEO

ChIP-seq of H3K27me3 in Asxl1 or Asxl2 KO mice

Project description:The goals of this study are to identify H3K27me3 changes in Asxl1 or Asxl2 KO mice

2017-06-26 | GSE93165 | GEO

ChIP-seq of H3K4me1 and H3K4me3 in SKNO1 cells after knockdown of ASXL2

Project description:The goals of this study are to identify the changes of H3K4me1 and H3K4me3 in SKNO1 cells after knockdown of ASXL2

2017-06-26 | GSE84361 | GEO

Myeloid specific ASXL2 deletion limits diet induced obesity by regulating energy expenditure

Project description:We previously reported that global deletion of the Enhancer of Trithorax and Polycomb (ETP) gene, Asxl2, attenuates osteoclast differentiation and also completely protects mice from HFD-induced weight gain. To determine role of this gene specifically in myeloid compartment, ASXL2flox mice were bred with LysM cre (Asxl2LysM). Bone marrow-derived macrophages (BMM) were cultured for 2 days with or without Rank-ligand (RANKL). We characterized the transcriptomic profiles of BMMs and osteoclast by performing unbiased RNA-sequencing. The expression profiles of both macrophages and osteoclast was significantly distinct between two genotypes. In particular, Enrichr analysis of differentially expressed genes (DEG) reveals substantial downregulation of those associated with extracellular matrix (ECM) organization, collagen formation, cytokine-cytokine interaction and inflammatory response including genes encoding TNFα, MMPs and CXCLs, in Asxl2LysM BMMs. In contrast, cell cycle and mitosis related genes are upregulated. The fact that most of the dominant downregulated genes are also implicated in modulating adipose tissue inflammation and fibrosis, supports the concept that genetic deletion of ASXL2, in myeloid cells, may modify obesity.

2021-01-23 | GSE144180 | GEO

RNA-seq of primary patient AML samples

Project description:The goals of this study are to compare transcriptome profiling (RNA-seq) of patients BM with or without ASXL2 mutations.

2017-06-26 | GSE84359 | GEO

ASXL2 is recurrently mutated in t(8;21) AML and regulates hematopoietic development [RNA_Seq_Asxl2_mutant]

Project description:Chromosomal translocation t(8;21) (q22;q22) leading to generation of oncogenic RUNX1-RUNX1T1 (AML1-ETO) fusion is a cytogenetic abnormality observed in about 10% of acute myelogenous leukemia (AML). To uncover somatic mutations that cooperate with t(8;21)-driven leukemia, we performed targeted and whole exome sequencing of newly-diagnosed and relapsed AML samples. We identified high frequency of truncating alterations in ASXL2 along with recurrent mutations of KIT, TET2, MGA, FLT3, and DHX15 in this subtype of AML. To investigate in-depth the role of ASXL2 in normal and malignant hematopoiesis, we utilized a mouse model of ASXL2 deficiency. Loss of ASXL2 caused progressive hematopoietic defects characterized by myeloid cell expansion, splenomegaly, extramedullary hematopoiesis and poor reconstitution ability in transplantation models. A parallel analysis of young and >1-year old Asxl2-deficient mice revealed age-dependent changes in the hematopoietic compartment leading to perturbations affecting not only myeloid and erythroid differentiation but also maturation of lymphoid cells. Our studies also suggest that expression of truncated ASXL2 protein confers proliferative advantage to mouse myeloid progenitors. Overall, these findings establish a critical role of ASXL2 in maintaining steady state hematopoiesis and provide insights into how its loss/mutation primes leukemic growth of myeloid cells.

2018-12-01 | GSE106796 | GEO

ASXL2 is recurrently mutated in t(8;21) AML and regulates hematopoietic development [RNA_Seq_Asxl2_knockout]

2018-12-01 | GSE106797 | 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