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ABSTRACT: RNA-Seq of HeLa Trim28

PROVIDER: PRJNA925462 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23121176.fastq.gz	Fastqsanger.gz
	SRR23121177.fastq.gz	Fastqsanger.gz
	SRR23121178.fastq.gz	Fastqsanger.gz
	SRR23121179.fastq.gz	Fastqsanger.gz
	SRR23121180.fastq.gz	Fastqsanger.gz

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TRIM28 regulates RNA polymerase II promoter proximal pausing and entry into processive elongation

Project description:Analysis of total PolII and Ser2-phosphorylated PolII genomic occupancy in control-transfected (WT) or Trim28-knockdown (Trim28-KD) embryonic stem cells. Embryonic stem cells were transfected with luciferase siRNA (WT) or Trim28 siRNA (Trim28 KD) in duplicate experiments. 48 hrs after transfection, cells were crosslinked with formaldehyde, collected, lysed, and chromatin was fragmented with sonication. Total PolII or Ser2-phosphorylated PolII genomic occupancy in WT or Trim28 KD cells were determined by ChIP-seq.

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ChIP-seq of ADNP and TRIM28 in the U2OS cell line (Human Bone Osteosarcoma Epithelial Cells)

Project description:In order to investigate the functions of the zinc finger transcription regulator ZMYM2 and the different types of ZMYM2 binding complex with TRIM28 or ADNP, we generated the ChIP-seq data of ADNP or TRIM28 in U2OS cells.

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RNA-seq of the U2OS cell line (Human Bone Osteosarcoma Epithelial Cells) treated with ZMYM2, TRIM28 or ADNP knock down against the control conditions.

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Single cell RNA-seq from Trim28 ovary knockout and wildtype mice ovaries and testis

Project description:Single cell RNA-seq (scRNA-seq) from Trim28 ovary knockout and wildtype mice ovaries and testis to help elucidate the function of Trim28 in the adult mouse ovaries. The analysis revealed that loss of Trim28 in the adult mouse ovaries lead to a transcriptional repogramming of the Granulosa cells towards the Sertoli cell fate. Therefore, Trim28 has a function to maintain the adult ovarian cell identity

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TRIM28 repression of retrotransposon-based enhancers is necessary to preserve transcriptional dynamics in embryonic stem cells

Project description:TRIM28 (KAP1 - KRAB-associated protein 1) is critical for the silencing of endogenous retroviruses (ERVs) in embryonic stem (ES) cells. Here, we reveal that an essential impact of this process is the protection of cellular gene expression in early embryos from perturbation by cis-acting activators contained within these genetic invaders. In TRIM28-depleted ES cells, repressive chromatin marks at ERVs are replaced by histone modifications typical of active enhancers, stimulating transcription of nearby cellular genes, notably those harboring bivalent promoters. Correspondingly, ERV-derived sequences can repress or enhance expression from an adjacent promoter in transgenic embryos depending on their TRIM28-sensitivity in ES cells. TRIM28-mediated control of ERVs is therefore crucial not just to prevent retrotransposition, but more broadly to safeguard the transcriptional dynamics of early embryos. Analyses of transcriptional profiles and chromatin state in TRIM28 WT and KO cells

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ZMAT2 condensates regulate the alternative splicing of TRIM28 to promote the proliferation of hepatocellular carcinoma cells

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