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RNA-seq (PolyA) of RNA from Tet-inducible SaOS2-p21 cells

ABSTRACT: RNA-seq (PolyA) of RNA from Tet-inducible SaOS2-p21 cells

PROVIDER: PRJNA528463 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8761740.fastq.gz	Fastqsanger.gz
	SRR8761735.fastq.gz	Fastqsanger.gz
	SRR8761736.fastq.gz	Fastqsanger.gz
	SRR8761737.fastq.gz	Fastqsanger.gz
	SRR8761738.fastq.gz	Fastqsanger.gz

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RNA-seq (PolyA) of RNA from Tet-inducible SaOS2-p21 cells

Project description:RNA was extracted from SaOS2 cells harboring a tet-inducible p21 expression vector. 3 replicates from untreated and 3 replicates from 24h doxycycline-treated cells.

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Effect of CDK8/19 inhibitor Senexin A on p21-regulated gene expression in human HT1080 p21-9 cells with IPTG-inducible p21

Project description:p21 (CDKN1A) expression from an IPTG-inducible promoter in HT1080 p21-9 cells was previously shown to inhibit a set of genes, many of which are involved in cell cycle progression, and to upregulate another set of genes, some of which have been implicated in cancer and age-related diseases. We have now developed Senexin A, a small-molecule inhibitor of p21-induced transcription, which we found to be a selective inhibitor of CDK8 and CDK19. Here we tested the effect of Senexin A on the induction and inhibition of transcription by p21. In this dataset, we include microarray gene expression data from samples of HT1080 p21-9 cells that were either untreated, treated with p21-inducing IPTG alone, with Senexin A alone, or with IPTG and Senexin A. This experiment shows that Senexin A inhibits primarily the induction but not the inhibition of gene expression by p21.

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Inducible disruption of Tet genes results in myeloid malignancy, readthrough transcription, and a heterochromatin-to-euchromatin switch [polyA+ RNA-seq]

Project description:The three mammalian TET dioxygenases oxidize the methyl group of 5-methylcytosine (5mC) in DNA, and the oxidised methylcytosines are essential intermediates in all known pathways of DNA demethylation. To define the in vivo consequences of complete TET deficiency, we inducibly deleted all three Tet genes in the mouse genome. Tet1/2/3 inducible TKO (iTKO) mice succumbed to acute myeloid leukaemia by 4-5 weeks. Single-cell RNA sequencing of Tet iTKO bone marrow cells revealed the appearance of new myeloid cell populations characterised by a striking increase in expression of all members of the stefin/cystatin gene cluster on mouse chromosome 16. In patients with acute myeloid leukaemia, high stefin/cystatin gene expression correlates with poor clinical outcomes. Increased expression of the clustered stefin/cystatin genes was associated with a heterochromatin-to-euchromatin compartment switch with readthrough transcription downstream of the clustered stefin/cystatin genes as well as other highly expressed genes but only minor changes in DNA methylation. Our data highlight new roles for TET enzymes that are distinct from their established function in DNA demethylation, and instead involve increased transcriptional readthrough and changes in three-dimensional genome organisation.

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TET-Mediated DNA Demethylation is Required for Inducible Vasculogenic Reprogramming of the Skin

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