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Transcriptome analysis of UHRF1 KO osteosarcoma cell lines

ABSTRACT: Transcriptome analysis of UHRF1 KO osteosarcoma cell lines

PROVIDER: PRJNA603580 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10982131_1.fastq.gz	Fastqsanger.gz
	SRR10982131_2.fastq.gz	Fastqsanger.gz
	SRR10982132_1.fastq.gz	Fastqsanger.gz
	SRR10982132_2.fastq.gz	Fastqsanger.gz
	SRR10982133_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of UHRF1 KO osteosarcoma cell lines

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Chromatin accessibility analysis of UHRF1 KO osteosarcoma cell lines

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Chromatin accessibility analysis of UHRF1 KO osteosarcoma cell lines

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RNA sequencing of WT and Uhrf1 KO iNKT cells

Project description:Deletion of Uhrf1 resulted in stage 1-specific defects during iNKT cell development. To investigate the molecular mechanism, we sorted WT and Uhrf1-KO stage 1 iNKT cells and performed RNA-seq. By comparing gene expression profile, we found metabolic defects in Uhrf1-KO stage 1 iNKT cells. The expression of CD71 (Tfrc), two subunits of CD98 (Slc3a2 and Slc7a5) and Glut3 (Slc2a3) was reduced in stage 1 iNKT cells. Besides, the downstream pathways of AKT-mTOR axis were significantly reduced. Collectively, our results suggest that Uhrf1 is required for iNKT cell development by regulating the Akt-mTOR signaling pathway. We first sorted WT and Uhrf1-KO stage 1 iNKT cells, extracted the mRNA and performed RNA-seq. We then analyzed the differentially expressed genes and performed KEGG pathway analysis. We used RT-PCR to verify the expression of the key nutrient related genes (Tfrc, Slc3a2, Slc7a5 and Slc2a3) and used flow cytometry to test the protein level of metabolic related molecules. Besides, we also analyzed the expression of genes of mTOR downstream pathways to demonstrate that Uhrf1 mediated AKt-mTOR axis regulates iNKT cell development.

2016-03-10 | E-GEOD-77941 | biostudies-arrayexpress

RNA sequencing of WT and Uhrf1 KO iNKT cells

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Transcriptome analysis to UHRF1 depletion in RaeL cells

Project description:RNAseq was used to identify host and viral transcriptome changes in UHRF1 knock-out RaeL cells. UHRF1 KO RaeL cells were subjected to FACSort for ICAM1+ subpopulations, which were further used for RNAseq analysis. The RaeL cells expressing control sgRNA was used as the control.

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Transcriptome analysis to UHRF1 depletion in MUTU I cells

Project description:RNAseq was used to identify host and viral transcriptome changes in UHRF1 knock-out MUTU I cells. UHRF1 KO MUTU I cells were subjected to FACSort for ICAM1+/GP350- and ICAM1-/GP350+ subpopulations, which were further used for RNAseq analysis. The MUTU I cells expressing control sgRNA was used as the control.

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RNA-seq analysis of gene expression profile in Uhrf1 WT and KO germinal center B cells

Project description:The goals of this study are to compare gene expression profiles of Uhrf1 WT and KO germinal center B cells and reveal the underlying mechanisms by which Uhrf1 regulates germinal center B cell responses. We found that upon Uhrf1 depeletion in germinal center B cells, most of the differentially expressed genes were upreguated.

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Expression data from HeLa cell lines stably expressing shRNA targeting ctrl or UHRF1

Project description:We used microarrays to explore the expression profile from cells expressing wild type and UHRF1 S674A mutant. HeLa cells expressing UHRF1 WT and S674A mutant showed similar gene expression pattern without significant affecting the transcription of DNA repari genes. UHRF1 was depleted in HeLa cells by shRNA treatment. Total RNA was purified and used to determine the global gene transcription profiles by microarray assays. The UHRF1-related genes expression profiles were compared among control cells, UHRF1-depleted cells, UHRF1 WT reconstituting cells and UHRF1 S674A mutant reconstituting cells.

2016-01-05 | E-GEOD-73751 | biostudies-arrayexpress

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