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Next generation sequencing of a unique set of glycovariant MC38 mouse colorectal cancer cell lines generated with CRISPR-Cas9 and CRISPR-dCas-VPR technology

ABSTRACT: Next generation sequencing of a unique set of glycovariant MC38 mouse colorectal cancer cell lines generated with CRISPR-Cas9 and CRISPR-dCas-VPR technology

PROVIDER: PRJNA601332 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10897438.fastq.gz	Fastqsanger.gz
	SRR10897439.fastq.gz	Fastqsanger.gz
	SRR10897440.fastq.gz	Fastqsanger.gz
	SRR10897441.fastq.gz	Fastqsanger.gz
	SRR10897442.fastq.gz	Fastqsanger.gz

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Next generation sequencing of a unique set of glycovariant MC38 mouse colorectal cancer cell lines generated with CRISPR-Cas9 and CRISPR-dCas-VPR technology

Project description:To investigate the effect of different tumor-associated glycans, mouse colorectal cancer cells (MC38 cell line) were genetically modified using CRISPR-Cas9 and CRISPR-dCas-VPR technology targeting different genes involved in glycosylation pathways. To study the effect of altered glycosylation at the transcriptional level, next generation sequencing was performed on the entire panel of glycovariant MC38 cell lines. The MC38 knockout cell lines created with the CRISPR-Cas9 technology are: MC38-MOCK#1, MC38-CMAS KO, MC38-COSMC KO, MC38-CMAS+COSMC KO. The MC38 overexpressing cell lines generated with the CRISPR-dCas9-VPR technology are: MC38-MOCK#2, MC38-FUT4, MC38-FUT9. Details on the cell lines can be found in the corresponding manuscript(s).

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Effects of inducible HIV-1 Vpr protein on cellular gene expression

Project description:Three 293 cell-derivative cell line were constructed using commercially available Invitrogen Flp-In TREx 293 cells. The cell lines express wild type HIV-1 Vpr and two mutant Vprs, F72A/R73A and R80A. The mutant Vprs are defective in the Vpr cell cycle arrest phenotype. The cell lines were characterized for their ability to express Vpr at the RNA and protein levels and functionally for the ability of the inducibly expressed Vprs to arrest cell cycle progression at G2/M. To study whether certain host cell genes showed alterations in expression following induced expression of Vpr, we conducted a large scale host cell gene expression profiling study using microarray technologies. To determine whether the differential expression of certain genes was associated with Vpr-induced cell cycle arrest, we compared the gene expression pattern of wild type Vpr expressing cells with the pattern of Vpr mutant F72A/R73A- or R80A-Vpr expressing cells. Doxycycline-induced and uninduced and Flp-In TREx 293/Vpr cells were collected 0, 1, 2, 4, 6, 8, 12, 16 and 24 hours post induction (hpi). Doxycyclineinduced and uninduced Flp-In TREx 293/Blank cells were also collected as a reference for following experiments. Total RNA was isolated using RNAeasy Midi Kit (QIAGEN), according to the manufacturer's protocol. Human long oligonucleotide microarrays were obtained from the National Cancer Institute Microarray Facility, Advanced Technology Center (Gaithersburg, MD). The microarrays (Hs Operon V2) contained 22,434 oligonucleotide (60-70 mer) spots on a glass slide. 25 µg of total RNAs isolated from doxycycline-induced Flp-In TREx 293 stably transfected blank- and FLAG tagged-Vpr cells were reverse transcribed using an oligo (dT) primer and aminoallyl-dNTP (Amersham Pharmacia). Unincorporated dNTPs were removed with QIAquick PCR purification kit (QIAGEN). Purified cDNA was processed for coupling reaction with Cy 5 or Cy 3-ester dye, respectively. Keywords: other

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Project description:Exploiting CRISPR-Cas9 technology to investigate individual histone modifications

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Transcriptomic analysis of Pepck-Vpr mouse kidney

Project description:We analyzed the transcriptomic profiles Pepck-Vpr mouse kidney by single-nuclear RNA-seq.

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The specificity of gene activation was revealed by RNA-seq in the HEK293T cells transfected with the dCasMINI-VPR or dhpCasMINI-VPR system targeting IL1RN [RNA-seq]

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Project description:MC38 tumors resistant to anti-PD-1 treatment (MC38-resistant) were generated through serial in vivo passaging, and global gene expression analysis was used to compare resistant and parental tumors. MC38 and MC38-resistant tumors exhibited widespread changes in global gene expression.

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Immunopeptidome on MC38 Cell line

Project description:PTM – driven antigenicity – immunopeptidome of MC38 cell line

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2024-08-23 | GSE253779 | GEO

Expression data from human monocyte derived macrophages infected with adenovirus expressing HIV-1 Vpr

Project description:HIV-1 Vpr protein is a multifunctional protein which perturbs human transcriptome and interacts with a number of cellular proteins. In this study, we have attempted to explore the efffects of Vpr on human transcriptome and have identified several genes which are involved in innate immune respone and cell signaling pathways. We used the microarray analysis to elucidate the differnetail expression pattern of differnet genes in human macrophages infected with HIV-1 Vpr. As result we found that HIV-1 Vpr protein leads to the induction of various interferon stimualted genes (ISGs) and chemokines in human macrophages. Human monocytes-derived macrophages (MDMs) were isolated from peripheral blood mononuclear cells (PBMCs) from two healthy donors and were infected with recombinant adenoviruses either expressing HIV-1 Vpr or ZsGreen1 as a control. At 48 hours post-infection, RNA was isolated and subjected to microarray analysis.

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Massive Proteome Remodelling by HIV Vpr

Project description:Viruses target host proteins for degradation to enhance their replication and transmission, and identifying these targets has provided key insights into the host-pathogen interaction1-3. Here, we use complementary unbiased mass spectrometry-based approaches to dissect the widespread proteomeic remodelling seen in HIV-1 infected T-cells. Remarkably, the HIV accessory protein Vpr is both necessary and sufficient to cause the vast majority of these changes. Protein regulation requires recruitment of the DCAF1/DDB1/CUL4 E3 ubiquitin ligase complex, and pulsed-Stable Isotope Labelling with Amino Acids in Cell Culture (SILAC) and immunoprecipitation-mass spectrometry (IP-MS) identified at least 38 cellular proteins directly targeted for degradation by Vpr. Whilst other HIV-1 accessory proteins downregulate a small number of specific host factors, Vpr depletes multiple protein targets, causing systems-level changes to the cellular proteome. A subset of the novel cellular targets identified in this study are depleted by Vpr variants from across HIV-1/SIVcpz and other primate lentiviral lineages, confirming their biological importance in vivo.

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