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USP7 shRNA knock-down in T-ALL cells [Jurkat_HSB2_shRNA_RNA-seq]

ABSTRACT: USP7 shRNA knock-down in T-ALL cells [Jurkat_HSB2_shRNA_RNA-seq]

PROVIDER: PRJNA624873 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11539212_1.fastq.gz	Fastqsanger.gz
	SRR11539212_2.fastq.gz	Fastqsanger.gz
	SRR11539213_1.fastq.gz	Fastqsanger.gz
	SRR11539213_2.fastq.gz	Fastqsanger.gz
	SRR11539214_1.fastq.gz	Fastqsanger.gz

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USP7 shRNA knock-down in T-ALL cells [Jurkat_HSB2_shRNA_RNA-seq]

Project description:RNAseq analysis of USP7 shRNA KD in T-ALL cell lines. USP7 shRNAs lentivirus was generated by co-transfecting 293T cells with shRNA vectors (OriGene or Sigma). T-ALL cells were transduced with USP7 shRNA lentivirus and sorted for GFP positive cells five days after transduction or selected by puromycin.

2021-03-09 | GSE148522 | GEO

Expression analysis of THP1 cells following shRNA knock-down of RUVBL2

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YG001: A Usp7-Tip60 pathway regulates early adipogenesis

Project description:USP7, a dominant DUB activity in 3T3-L1 adipocytes and in mouse adipose tissue, increases Tip60 protein levels, and deubiquitinates Tip60 both in intact cells and in vitro. Treatment with a pan deubiquitinase (DUB) inhibitor, or knockdown of USP7, decreases adipogenesis. Transcriptome analysis reveals a common set of cell cycle genes to be co-regulated by both Tip60 and USP7. Knock down of either factor results in impaired mitotic clonal expansion, an early step in adipogenesis. These results therefore reveal deubiquitination of a transcriptional coregulator to be a key mechanism in the regulation of early adipogenesis Mature 3T3-L1 adipocytes were subjected to RNAi-mediated knock down with control(C), USP7(U)- or Tip60(T)-specific oligonucleotides. For this, 4 replicates of differentiated 3T3-L1 cells were transfected with Amaxa technology. Two days after transfection cells were washed twice with PBS twice and lysed in 0.5ml Trizol (Invitrogen). mRNA expression of Tip60 and USP7 was assessed by qRT-PCR. Amplified cRNA samples were labeled with either cy3 or cy5 and put on microarray together with and oppositely labeled common reference sample consisting of cRNA derived from undifferentiated 3T3-L1 cells.

2013-08-28 | E-GEOD-28587 | biostudies-arrayexpress

FGFR3 knock-down

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SPARC knock down

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Heterozygous and Homozygous Knock-Out of USP7 mouse models [mouse_RNA-seq]

Project description:RNAseq analysis of USP7 conditional knock-out (cKO) mice. They were designed to flox exon 6 of USP7 and to allow deletion of exon 6 upon expression of Cre recombinase 27. USP7FL/FL mice were bred with Vav1-Cre mice to obtain USP7FL/wt-Vav1-Cre mice (heterozygote). USP7FL/FL-Vav1-Cre mice (homozygote) were obtained via breeding of heterozygous cKO mice.

2021-03-09 | GSE148521 | GEO

USP7 CRISPR knock-out in T-ALL cells [Molt4_CRISPR_RNA-seq]

Project description:USP7 CRISPR knock-out in T-ALL cells [Molt4_CRISPR_RNA-seq]

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Transcription profiling of mouse G1ME cells following retroviral infection and shRNA-mediated knock-down of Suz12 and Ezh2

Project description:Suz12 in hematopoiesis II. Retroviral Infection and shRNA-mediated knock-down of Suz12 and Ezh2 in mouse G1ME cells.

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shRNA-mediated knock down of Bmi-1 and Mel-18 in medulloblastoma cells

Project description:Bmi-1 and Mel-18 are close structural homologues that belong to the polycomb group (PcG) of transcriptional regulators of homeotic gene expression in development. They are believed to stably maintain repression of gene expression by altering the state of chromatin at specific promoters. A number of clinical and experimental observations have also implicated Bmi-1 in tumorigenesis and stem cell maintenance. Bmi-1 overexpression or amplification has been observed in a number of human malignancies, particularly in B-cell lymphomas, medulloblastomas and breast cancer. We report here that shRNA-mediated knock-down of either Bmi-1 or Mel-18 in human medulloblastoma DAOY cells results in the inhibition of proliferation, loss of clonogenic survival and anchorage-independent growth, and suppression of xenograft tumor formation in nude mice. Furthermore, overexpression of both Bmi-1 and Mel-18 significantly increased clonogenic survival of Rat1 fibroblasts. In contrast, stable downregulation of Bmi-1 or Mel-18 alone did not affect the growth of SK-OV-3 or U2OS cancer cell lines or normal human WI38 fibroblasts. Gene expression analysis of shRNA-expressing DAOY cells has demonstrated a significant overlap in the Bmi-1- and Mel-18-regulated genes and revealed novel gene targets under their control. Taken together, these results suggest that Bmi-1 and Mel-18 might have overlapping functions in human tumorigenesis. Keywords: shRNA knock-down

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RNAseq analysis of USP7 knockdown in MM16 and MM27 metastatic melanoma PDX cells

Project description:Purpose: Study of transcriptomic changes upon depletion of USP7 Methods: Melanoma PDX cells were transduced with lentiviral vectors expressing Scrambled(shSCR) or USP7 targeting (shUSP7) shRNA

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