Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of neural crest progenitor cultures derived from human embryonic stem cells carrying nonsense mutations in the Polycomb gene ASXL1 [HET]

ABSTRACT: Gene expression profiling of neural crest progenitor cultures derived from human embryonic stem cells carrying nonsense mutations in the Polycomb gene ASXL1 [HET]

PROVIDER: PRJNA524641 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8643790.fastq.gz	Fastqsanger.gz
	SRR8643800.fastq.gz	Fastqsanger.gz
	SRR8643791.fastq.gz	Fastqsanger.gz
	SRR8643792.fastq.gz	Fastqsanger.gz
	SRR8643793.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Gene expression profiling of neural crest progenitor cultures derived from human embryonic stem cells carrying nonsense mutations in the Polycomb gene ASXL1 [HET]

Project description:We observed impaired neural crest cell differentiation from human embryonic stem cells that harbor nonsense mutations in the Polycomb gene ASXL1. To investigate the underlying molecular mechanisms, we harvested neural crest differentiation cultures from wildtype and heterozygous ASXL1 mutant lines at day 7 of a neural crest differentiation protocol and performed total RNA sequencing using the Illumina HiSeq2500 system. Analyses of global transcriptomes revealed profound changes between wildtype and mutant cultures, and we identified downregulation of the neural crest transcription factor ZIC1.

2019-04-23 | GSE127268 | GEO

Gene expression profiling of neural crest progenitor cultures derived from human embryonic stem cells carrying nonsense mutations in the Polycomb gene ASXL1 [HOM]

Project description:We observed impaired neural crest cell differentiation from human embryonic stem cells that harbor nonsense mutations in the Polycomb gene ASXL1. To investigate the underlying molecular mechanisms, we harvested neural crest differentiation cultures from wildtype and homozygous ASXL1 mutant lines at day 7 of a neural crest differentiation protocol and performed total RNA sequencing using the Illumina NextSeq system. Analyses of global transcriptomes revealed profound changes between wildtype and mutant cultures, and we identified downregulation of several genes of the neural crest regulatory network, most prominently of the transcription factor ZIC1.

2019-04-23 | GSE120200 | GEO

Gene expression profiling of neural crest progenitor cultures derived from human embryonic stem cells carrying nonsense mutations in the Polycomb gene ASXL1

Project description:Gene expression profiling of neural crest progenitor cultures derived from human embryonic stem cells carrying nonsense mutations in the Polycomb gene ASXL1

| PRJNA524639 | ENA

Gene expression profiling of neural crest progenitor cultures derived from human embryonic stem cells carrying nonsense mutations in the Polycomb gene ASXL1 [HOM]

Project description:Gene expression profiling of neural crest progenitor cultures derived from human embryonic stem cells carrying nonsense mutations in the Polycomb gene ASXL1 [HOM]

| PRJNA491940 | ENA

RNA sequencing of zebrafish asxl1+/+ and asxl1-/-

Project description:ASXL1 gene is one of the most frequently mutated genes in malignant myeloid diseases. In patients, ASXL1 mutations are usually heterozygous frameshift or non-sense mutations leading to C-terminal truncation. Here, we generated an endogenous C-terminal truncated Asxl1 mutant in zebrafish which is more comparable to human malignant leukemia patients. Our data showed that at embryonic stage, neutrophil differentiation was explicitly blocked in our mutant. To understand the basis for the impairment of neutrophil differentiation in zebrafish asxl1 mutants, we performed RNA-seq of asxl1 mutants at 3dpf and their littermate controls. Similar with the phenotype we observed, the expression of neutrophil markers were all included in down-regulated genes. Nonetheless, the expression of myeloid progenitor marker and macrophage marker were not impaired in asxl1 mutants. We also found inflammatory cytokine and matrix metalloproteinases were upregulated after mutated asxl1. It suggests that neutrophil deficiency may stimulate the expression of some inflammatory cytokines and enhances the inflammatory responds. Therefore, transcriptome analysis mainly represented the disruption of neutrophil development.

2021-08-04 | GSE142214 | GEO

RNA sequencing of zebrafish asxl1+/+ and asxl1-/-

Project description:RNA sequencing of zebrafish asxl1+/+ and asxl1-/-

| PRJNA596232 | ENA

Cancer-associated ASXL1 mutations may act as gain-of-function mutations of the ASXL1-BAP1 complex

Project description:ASXL1 is the obligate regulatory subunit of a deubiquitinase complex whose catalytic subunit is BAP1. Heterozygous mutations of ASXL1 that result in premature truncations are frequent in myeloid leukemias and Bohring-Opitz syndrome. Here, we demonstrate that truncated ASXL1 proteins confer enhanced activity on the ASXL1-BAP1 complex. Stable expression of truncated, hyperactive ASXL1-BAP1 complexes in a hematopoietic precursor cell line resulted in global erasure of H2AK119Ub, striking depletion of H3K27me3, selective upregulation of a subset of genes whose promoters bore both H2AK119Ub and H3K4me3, and spontaneous differentiation to the mast cell lineage. These outcomes required the catalytic activity of BAP1, indicating these events were downstream consequences of H2AK119Ub erasure. In bone marrow precursors, truncated ASXL1-BAP1 expression cooperated with TET2 loss-of-function to increase differentiation to the myeloid lineage in vivo. We propose that pathological ASXL1 mutations confer gain-of-function on the ASXL-BAP1 complex. ChIP-Seq for H2AK119Ub, H3K4me3, H3K27me3 on EML cells. RNA-Seq on EML cells expressing ASXL1(1-479)+BAP1 and control.

2015-03-11 | E-GEOD-65555 | biostudies-arrayexpress

Gene expression profiles of mutant ASXL1 knock-in HSPCs

Project description:To assess the effect of mutant ASXL1 (ASXL1-MT) on gene expression and RNA splicing in hematopoietic cells, we performed RNA-seq using HSPCs (bone marrow lineage-, c-Kit+ cells) derived from control or ASXL1-MT-KI mice.

2021-07-05 | GSE179375 | GEO

ASXL1 Mutations Promote Myeloid Transformation Through Loss of PRC2-Mediated Gene Repression

Project description:Recurrent somatic ASXL1 mutations occur in patients with myelodysplasia (MDS), myeloproliferative neoplasms (MPN), and acute myeloid leukemia (AML), and are associated with adverse outcome. Despite the genetic and clinical data implicating ASXL1 mutations in myeloid malignancies, the mechanisms of transformation by ASXL1 mutations are not understood. Here we identify that ASXL1 mutations result in loss of PRC2-mediated histone H3 lysine 27 (H3K27) tri-methylation. Through integration of microarray data with genome-wide histone modification ChIP-Seq data we identify targets of ASXL1 repression including the posterior HOXA cluster that is known to contribute to myeloid transformation. We demonstrate that ASXL1 associates with the Polycomb repressive complex 2 (PRC2), and that loss of ASXL1 in vivo collaborates with NRASG12D to promote myeloid leukemogenesis. To assess the genome-wide effects of ASXL1 loss on chromatin state we performed chromatin immunoprecipitation followed by next generation sequencing (CHIP-seq) for histone modifications known to be associated with PcG (histone H3 lysine 27 trimethylation (H3K27me3)) or TxG activity (histone H3 lysine 4 trimethylation (H3K4me3)) in UKE1 cells expressing empty vector (EV) or 2 independent validated shRNAs for ASXL1. This Series represents the ChIP-Seq data (not the microarray data referenced in the summary above). The related micorarray data are available in GEO as GSE38692.

2012-08-21 | E-GEOD-38861 | biostudies-arrayexpress

Asxl1 and Cebpa cooperation in AML revealed by a novel Asxl1 mutant mouse model

Project description:Asxl1 is one of the most commonly mutated genes in malignancies including myelodysplastic syndromes (MDS) and Acute Myeloid Leukemia (AML). We generated a mouse model that harbors the most common mutation on ASXL1 gene detected in MDS patients: c.1934dupG, p.G646WfsX12 at the endogenous murine Asxl1 locus: the G643WfsX12 mutant, from here on referred as Asxl1G643W. Mutations on Asxl1 co-occur with mutations on CEBPA in AML patients, therefore, in order to understand how Asxl1 and Cebpa co-operate, we set up to cross our Cebpa-p30 mutant mouse model with our newly generated Asxl1 G643Wfs12 mutant. In this study we provided mechanistic information about the cooperation between these two factors. Furthermore, our mouse model proved able to recapitulate the chemotherapy response of human patients with Asxl1 mutations, thus representing a potent tool for future preclinical studies focusing on Asxl1 mutant AML.

2020-05-12 | GSE133314 | 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