Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A novel tumor suppressing role for RUNX3 is shown where a direct interaction with MYC leads to disruption of MYC-MAX heterodimers and consequent degradation of the MYC oncoprotein

ABSTRACT: A novel tumor suppressing role for RUNX3 is shown where a direct interaction with MYC leads to disruption of MYC-MAX heterodimers and consequent degradation of the MYC oncoprotein

PROVIDER: PRJNA977962 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24771600_1.fastq.gz	Fastqsanger.gz
	SRR24771600_2.fastq.gz	Fastqsanger.gz
	SRR24771601_1.fastq.gz	Fastqsanger.gz
	SRR24771601_2.fastq.gz	Fastqsanger.gz
	SRR24771602_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

A novel tumor suppressing role for RUNX3 is shown where a direct interaction with MYC leads to disruption of MYC-MAX heterodimers and consequent degradation of the MYC oncoprotein

Project description:Developmental regulator RUNX3 targets MYC protein for rapid degradation through the glycogen synthase kinase-3 beta-box/WD repeat-containing protein 7 (GSK3β-FBXW7) proteolytic pathway. We therefore uncover a previously unknown mode of MYC destabilization by RUNX3 and provide an explanation as to why RUNX3 inhibits early-stage cancer development in gastrointestinal and lung mouse cancer models.

2023-06-24 | GSE233777 | GEO

The interactomes of RUNX1 and RUNX3 from Mus musculus T cells

Project description:Cellular binary fate decisions require the progeny to silence genes associated with the alternative fate. The major subsets of alpha:beta T cells have been extensively studied as a model system for fate decisions. While the transcription factor RUNX3 is required for the initiation of Cd4 silencing in CD8 T cell progenitors, it is not required to maintain the silencing of Cd4 and other helper T lineage genes. The other runt domain containing protein, RUNX1, silences Cd4 in an earlier T cell progenitor, but this silencing is reversed whereas the gene silencing after RUNX3 expression is not reverse. Therefore, we hypothesized that RUNX3 and not RUNX1 recruits other factors that maintains the silencing of helper T lineage genes in CD8 T cells. To this end, we performed a proteomics screen of RUNX1 and RUNX3 to determine candidate silencing factors.

2019-11-12 | PXD007511 | Pride

RNA-seq of E11.5 TrkC neurons of Runx3-P2+/- and Runx3-P2-/- mice

Project description:To gain insight into the role of Runx3 in TrkC neurons we performed RNA-seq on E11.5 TrkC neurons isolated from cervical ganglia of Runx3-P2+/- and Runx3-P2-/- mice

2016-11-20 | GSE81140 | GEO

RUNX3 Facilitates Growth of Ewing Sarcoma Cells

Project description:Ewing sarcoma is an aggressive pediatric small round cell tumor that predominantly occurs in bone. Approximately 85% of Ewing sarcomas harbor the EWS/FLI fusion protein, which arises from a chromosomal translocation, t(11:22)(q24:q12). EWS/FLI interacts with numerous lineage-essential transcription factors to maintain mesenchymal progenitors in an undifferentiated state. We previously showed that EWS/FLI binds the osteogenic transcription factor RUNX2 and prevents osteoblast differentiation. In this study, we investigated the role of another Runt-domain protein, RUNX3, in Ewing sarcoma. RUNX3 participates in mesenchymal-derived bone formation and is a context dependent tumor suppressor and oncogene. RUNX3 was detected in all Ewing sarcoma cells examined, whereas RUNX2 was detected in only 73% of specimens. Like RUNX2, RUNX3 binds to EWS/FLI via its Runt domain. EWS/FLI prevented RUNX3 from activating the transcription of a RUNX-responsive reporter, p6OSE2. Stable suppression of RUNX3 expression in the Ewing sarcoma cell line A673 delayed colony growth in anchorage independent soft agar assays and reversed expression of EWS/FLI-responsive genes. These results demonstrate an important role for RUNX3 in Ewing sarcoma. RNA-seq to compare transcriptiome of control A673 ewing sarcoma cells stably expression a non-target or RUNX3 shRNA

2014-05-01 | E-GEOD-56900 | biostudies-arrayexpress

Runx3 function in splenic NK cells

Project description:NK cells are innate immune cells that recognize and kill foreign, virally-infected and tumor cells without the need for prior immunization. NK expansion following viral infection is IL-2 or IL-15-dependent. To identify Runx3 responsive genes, NK cells were isolated from spleen of WT and Runx3-/- mice . Six samples (3 WT and 3 Runx3-/-) of freshly isolated NK cells (resting) were separately obtained from individual mice.

2013-11-18 | E-GEOD-50123 | biostudies-arrayexpress

Runx3 function in CD8+ splenic T cells

Project description:CD8+T cells are immune cells that recognize foreign antigens on infected and tumor cells, leading to cytokine-dependent expansion and activation of cytotoxicity towards the targets. To identify Runx3 responsive genes, CD8+ T cells were isolated from spleen of WT and Runx3-/- mice . Six samples (3 WT and 3 Runx3-/-) of freshly isolated CD8+ T cells (resting) were separately obtained from individual mice.

2013-11-18 | E-GEOD-50119 | biostudies-arrayexpress

Myc correlates globally with transcription complexes rather than specific DNA elements

Project description:The Myc-Max heterodimer has been thought of as a sequence specific DNA binding protein that regulates transcription of a large number of genes. We demonstrate here that the positions of the human genome occupied by Myc-Max correlate with the RNA polymerase II (Pol II) transcription complex rather than to the canonical DNA binding sequence element CACGTG. The heterodimer is positioned slightly upstream of essentially all promoter proximal paused polymerases and is found throughout the transcribed regions of genes. Using a multi-genome analysis of promoter regions we show that the heterodimers are oriented with respect to the direction of transcription with Myc downstream of Max. In strong support of a model in which the Myc is recruited by transcription complexes rather than specific DNA sequences, we found that the difference in affinities of Myc-Max heterodimers for CACGTG versus non-specific DNA is not great enough to drive the pattern of genome occupancy exhibited. A total of 2 ChIP-Seq data for Myc and Max in human HeLa cell.

2013-01-02 | E-GEOD-43227 | biostudies-arrayexpress

Loss of Runx3 in osteoblasts provokes severe congenital osteopenia

Project description:Murine Runx3 is expressed in developing bone osteoblasts (OBLs) and its deletion in these cells culminates in severe congenital osteopenia. We demonstrate that Runx3 is non-redundantly involved in the proliferation of early pre-committed OBL progenitor cells, a critical step in the generation of adequate numbers of bone-forming OBLs. Thus, in the absence of Runx3 in cells of this lineage, the number of mature/active OBLs is significantly diminished, providing a mechanistic explanation to the observed osteopenia. This experiment was aimed at identifying genes that are likely regulated by Runx3 along osteoblastogenesis. To elucidate the Runx3-mediated transcriptional program along OBL differentiation, we compared gene expression profile in WT and Runx3f/f/Col1a1-cre calvarial OBLs. Progenitor cells were purified and RNA extracted, reverse-transcribed, fragmented, labeled and hybridized to GeneChipÂ® Mouse Gene 2.0 ST Array.

2014-05-01 | E-GEOD-57195 | biostudies-arrayexpress

Multiple interactions of the oncoprotein transcription factor MYC with the SWI/SNF chromatin remodeler

Project description:Multiple interactions of the oncoprotein transcription factor MYC with the SWI/SNF chromatin remodeler

| PRJNA692456 | ENA

Runx3 function in CD4+ splenic dendritic cells

Project description:CD4+ dendritic cells are part of the innate immunity essential for priming and activating of CD4+ T cells To identify Runx3 responsive genes CD4+ dendritic cells were sorted from freshly isolated macs enriched splenic DCs taken from 6 weeks old mice. Six samples from six mice were sorted and analyzed where in each littermates pair consisted of a control and Runx3 KO.

2014-06-22 | E-GEOD-48589 | 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