Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Fli1+ cells transcriptional analysis reveals LMO2-PRDM16 axis in angiogenesis

ABSTRACT: Different GFP+ cell population were isolated from Tg(fli1:EGFP) zebrafish embryos. Novel roles of epigenetic modifiers in endothelial differentiation were identified.

ORGANISM(S): Danio rerio

PROVIDER: GSE149152 | GEO | 2021/07/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Fli1<sup>+</sup> cells transcriptional analysis reveals an Lmo2-Prdm16 axis in angiogenesis.

Project description:A network of molecular factors drives the development, differentiation, and maintenance of endothelial cells. Friend leukemia integration 1 transcription factor (FLI1) is a bona fide marker of endothelial cells during early development. In zebrafish Tg(fli1:EGFP)y1 , we identified two endothelial cell populations, high-fli1+ and low-fli1+, by the intensity of green fluorescent protein signal. By comparing RNA-sequencing analysis of non-fli1 expressing cells (fli1-) with these two (fli1+) cell populations, we identified several up-regulated genes, not previously recognized as important, during endothelial development. Compared with fli1- and low-fli1+ cells, high-fli1+ cells showed up-regulated expression of the zinc finger transcription factor PRDI-BF1 and RIZ homology domain containing 16 (prdm16). Prdm16 knockdown (KD) by morpholino in the zebrafish larva was associated with impaired angiogenesis and increased number of low-fli1+ cells at the expense of high-fli1+ cells. In addition, PRDM16 KD in endothelial cells derived from human-induced pluripotent stem cells impaired their differentiation and migration in vitro. Moreover, zebrafish mutants (mut) with loss of function for the oncogene LIM domain only 2 (lmo2) also showed reduced prdm16 gene expression combined with impaired angiogenesis. Prdm16 expression was reduced further in endothelial (CD31+) cells compared with CD31- cells isolated from lmo2-mutants (lmo2-mut) embryos. Chromatin immunoprecipitation-PCR demonstrated that Lmo2 binds to the promoter and directly regulates the transcription of prdm16 This work unveils a mechanism by which prdm16 expression is activated in endothelial cells by Lmo2 and highlights a possible therapeutic pathway by which to modulate endothelial cell growth and repair.

| S-EPMC8346798 | biostudies-literature

Fli1+ cells transcriptional analysis reveals LMO2-PRDM16 axis in angiogenesis

Project description:Fli1+ cells transcriptional analysis reveals LMO2-PRDM16 axis in angiogenesis

| PRJNA627467 | ENA

The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes developmental defects in zebrafish embryos

Project description:The fusion oncoprotein EWS-FLI1 arises from a t(11;22)(q24;q12) chromosomal translocation and causes Ewing's Sarcoma, a malignant bone tumor. The mechanism whereby EWS-FLI1 transforms cells is unknown. We made germline transgenic zebrafish expressing human EWS-FLI1 under the control of the heat shock promoter. Induction of EWS-FLI1 expression causes multiple defects in embryonic development. We compared gene expression in control and transgenic EWS-FLI1 zebrafish. The results identify a conserved set of EWS-FLI1-regulated genes, and provide insight into the pathogenesis of Ewing's Sarcoma tumors. We performed heat shock and isolated total RNA for microarray studies comparing wildtype AB strain zebrafish with transgenic zebrafish expressing human EWS-FLI1 [Tg(HSP:EWS-FLI1)]. RNA was biotin-lableled and hybridized to zebrafish-specific Affymetrix arrays.

2011-11-01 | E-GEOD-31185 | biostudies-arrayexpress

The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes Ewing's-type tumors in zebrafish

Project description:The fusion oncoprotein EWS-FLI1 arises from a t(11;22)(q24;q12) chromosomal translocation and causes Ewing's Sarcoma, a malignant bone tumor. The mechanism whereby EWS-FLI1 transforms cells is unknown. Somatic, mosaic expression of human EWS-FLI1 in zebrafish from the heat shock promoter [Tg(HSP:EWS-FLI1)] caused small round blue cell tumors (SRBCTs) similar to human Ewing's sarcoma. We performed microarray studies comparing zebrafish SRBCTs to another tumor type, zebrafish malignant peripheral nerve sheath tumors (MPNSTs). The results identify a conserved set of EWS-FLI1-regulated genes,and provide insight into the pathogenesis of Ewing's Sarcoma tumors. Zebrafish SRBCTs arising from somatic insertions of the EWS-FLI1 transgene were collected. MPNSTs from non-transgenic fish of the same genetic background were collected in parallel. RNA was prepared from all samples and hybridized to zebrafish-specific Affymetrix arrays.

2011-11-01 | E-GEOD-31186 | biostudies-arrayexpress

The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes Ewing's-type tumors in zebrafish

Project description:The fusion oncoprotein EWS-FLI1 arises from a t(11;22)(q24;q12) chromosomal translocation and causes Ewing's Sarcoma, a malignant bone tumor. The mechanism whereby EWS-FLI1 transforms cells is unknown. Somatic, mosaic expression of human EWS-FLI1 in zebrafish from the heat shock promoter [Tg(HSP:EWS-FLI1)] caused small round blue cell tumors (SRBCTs) similar to human Ewing's sarcoma. We performed microarray studies comparing zebrafish SRBCTs to another tumor type, zebrafish malignant peripheral nerve sheath tumors (MPNSTs). The results identify a conserved set of EWS-FLI1-regulated genes,and provide insight into the pathogenesis of Ewing's Sarcoma tumors.

2011-11-01 | GSE31186 | GEO

Differentially expressed genes in zebrafish vascular development

Project description:The goal of this experiment was to identify using tissue specific transgenic zebrafish (Fli:EGFP), genes of interest important for embryonic vascular development. Keywords: time course, GFP cell isolation, zebrafish The experiment contained 6 samples. A18, A24 = total RNA isolated from 18 and 24 hpf zebrafish embryo; B2, C and D2=RNA isolated from GFP positive cells sorted at 18, 24 and 28 hpf respectively from Tg(Fli1:EGFP) embryos; E2 = RNA isolated from GFP positive cells sorted at 18 hpf from Tg(Flk:GRCFP) embryos.

2010-05-22 | E-GEOD-12516 | biostudies-arrayexpress

A zebrafish transgenic model of Ewing's Sarcoma reveals conserved mediators of EWS-FLI1 tumorigenesis

Project description:This SuperSeries is composed of the following subset Series: GSE31185: The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes developmental defects in zebrafish embryos GSE31186: The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes Ewing's-type tumors in zebrafish Refer to individual Series

2011-11-01 | E-GEOD-31217 | biostudies-arrayexpress

The human Ewing's Sarcoma oncoprotein EWS-FLI1 causes developmental defects in zebrafish embryos

2011-11-01 | GSE31185 | GEO

Trancription factor Fli1 occupancy in Dnmt3aKO/FLT3-ITD lymphoid leukemia

Project description:We mapped binding of FLI1 in Dnmt3aKO/FLT3-ITD leukemias over-expressing Dnmt3a or GFP.

2016-05-19 | GSE80724 | GEO

USP9X stabilizes EWS-FLI1 to promote cancer cell growth in Ewing’s sarcoma

Project description:Ewing’s sarcoma (EWS) is a cancer of the bones or soft tissues in children and adolescents. EWS-FLI1 is a transcriptional factor and the key driver of EWS. To characterize the changes of downstream transcriptional profiles of EWS-FLI1 in A673 cells upon knockdown of EWS-FLI1 and deubiquitinase USP9X, RNA-seq was performed in A673 cells transfected with EWS-FLI1 esiRNA, USP9X esiRNA or GFP esiRNA as control. The data indicates that USP9X regulates transcriptional profiles of EWS through mediating EWS-FLI1.

2022-01-01 | GSE185429 | 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