Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-seq of ASXL2 in SKNO1 cells

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE84363 | GEO | 2017/06/26

SECONDARY ACCESSION(S): PRJNA329034

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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 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

ATAC-seq of AML1-ETO9 leukemias

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

2017-06-26 | GSE84364 | 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

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

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

Project description: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.

2017-06-26 | GSE84358 | GEO

CARM1-mediated methylation of ASXL2 impairs tumor suppressor gene activation by MLL3/COMPASS

Project description:An imbalance in the activities of the Polycomb and Trithorax complexes underlies numerous human pathologies, including cancer. The BAP1 deubiquitinase (DUB) complex negatively regulates Polycomb activity and also recruits the Trithorax histone H3K4 methyltransferase, MLL3/COMPASS, to the enhancers of tumor suppressor genes. We and others have demonstrated that the BAP1-MLL3 pathway is mutated in several differ cancers. Yet, how BAP1 recruits MLL3 to these loci remains a fundamentally important unanswered question. Here we demonstrate that ASXL2 directly mediates the interaction between the BAP1 complex and MLL3/COMPASS. ASXL2 loss abolishes the MLL3-BAP1 interaction, leading to decreased MLL3 occupancy at enhancers and reduced expression of BAP1-MLL3 target genes. The interaction between ASXL2 and MLL3 is negatively regulated by protein arginine methyltransferase 4 (PRMT4, also known as CARM1), which methylates ASXL2 on R639/R641. Methylation of ASXL2 by CARM1 blocks binding to MLL3 binding and impairs the expression of MLL3 dependent genes. This finding uncovers a novel transcription repression function for CARM1 and provides a unique insight into the BAP1/ASXL2/MLL3 axis, which is controlled by arginine methylation and could serve as a target for potential cancer therapeutics.

2022-08-12 | GSE182625 | GEO

Homo sapiens

Project description:ChIP-seq of ASXL2 in SKNO1 cells

| PRJNA329034 | ENA

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

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