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RNA-seq of Runx3 cKO SFZ/DZ chondrocytes.

ABSTRACT: RNA-seq of Runx3 cKO SFZ/DZ chondrocytes.

PROVIDER: PRJNA661298 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12582674.fastq.gz	Fastqsanger.gz
	SRR12582675.fastq.gz	Fastqsanger.gz
	SRR12582676.fastq.gz	Fastqsanger.gz
	SRR12582677.fastq.gz	Fastqsanger.gz
	SRR12582678.fastq.gz	Fastqsanger.gz

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RNA-seq of Runx3 cKO SFZ/DZ chondrocytes.

Project description:Purpose: To demonstrate Runx3's association with organizing the extracellular matrix in SFZ/DZ chondrocytes. Method: RNA samples were collected from SFZ/DZ chondrocytes of 5-day-old Col2a1-Cre;Runx3fl/fl and Runx3fl/fl mice. Results: 18 genes were up- or down-regulated by more than 2-fold in the Runx3 knockout in SFZ. Conclusions: However, genes organizing the extracellular matrix were down-regulated in Runx3 cKO DZ chondrocytes.

2020-09-04 | GSE157433 | GEO

ChIP-seq of Runx3 in SFZ chondrocytes.

Project description:Purpose: To demonstrate Runx3's association with organizing the extracellular matrix in SFZ chondrocytes. Method: Fragment DNA samples were collected by using Anti-FLAG or IgG, from SFZ chondrocytes treated with lipofection of RUNX3-FLAG Results: 21,730 raw peaks met the peak calling criterion. Conclusions: By GO analysis, the extracellular structure organization and collagen fibril organization terms were the most significantly enriched.

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ChIP-seq of Runx3 in SFZ chondrocytes.

Project description:ChIP-seq of Runx3 in SFZ chondrocytes.

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RNA-seq of Runx2 cKO primary chondrocytes.

Project description:Purpose: To demonstrate Runx2's association with organizing the extracellular matrix in primary chondrocytes. Method: RNA samples were collected from primary chondrocytes of 5-day-old Col2a1-CreERT2;Runx2fl/fl and Runx2fl/fl mice, cultured with or without IL-1beta. Results: Thirty-three genes cultured without IL-1beta and 45 genes with IL-1beta were up- or down-regulated by more than 2-fold in the Runx2 knockout in primary chondrocytes. Conclusions: Genes including collagen fibers were down-regulated in Runx2 cKO primary chondrocytes.

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Expression data from SFZ cells and costal chondrocytes

Project description:To understand difference between SFZ cells and costal chondrocytes, total RNAs from SFZ cells and costal chondrocytes were analyzed by microarray.

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RNA-seq of Runx2 cKO primary chondrocytes.

Project description:RNA-seq of Runx2 cKO primary chondrocytes.

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Next Generation Sequencing of Ezh2-cKO and Utx cKO transcriptomes of exostoses in mice

Project description:Ezh2-cKO or Utx-cKO in chondrocytes initiate metachondromatosis which containing both exostoses and enchondromas. To figure out whether the exostoses of Ezh2-cKO and Utx-cKO were the similar tumore, we compared the transcriptional profiles using RNA-sequencing of exostoses from Ezh2-cKO and Utx-cKO mice.

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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

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

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