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Analysis of transcriptomes of healthy donor and CD46 deficient CD8 T cells

ABSTRACT: Analysis of transcriptomes of healthy donor and CD46 deficient CD8 T cells

PROVIDER: PRJNA490705 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7826040.fastq.gz	Fastqsanger.gz
	SRR7826050.fastq.gz	Fastqsanger.gz
	SRR7826041.fastq.gz	Fastqsanger.gz
	SRR7826051.fastq.gz	Fastqsanger.gz
	SRR7826042.fastq.gz	Fastqsanger.gz

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Analysis of transcriptomes of healthy donor and CD46 deficient CD8 T cells

Project description:This SuperSeries is composed of the SubSeries listed below. We analyze the transcriptomes of healthy donor and CD46 deficieint patients with and without in vitro activation by microarray and RNA-seq

2018-09-14 | GSE119919 | GEO

Gene expression in T cells from CD46-deficient patients and matcherd healthy controls

Project description:Recent data indicate that intracellularly activated and autocrine-functioning complement activation fragments - in conjunction with an NLRP3 inflammasome - is critical for normal human Th1 induction and contraction. More specifically, engagement of of the C3aR and CD46 by autocrine generated C3a and C3b, respectively, drives the metabolic reprogramming needed for IFN-gamma secrtion by human CD4+ T cells. It was not clear whether autocrine complement and/or the NLRP3 inflammasome are also needed for normal human cytotoxic CD8+ T cell (CTL) responses. During this study, we used CTLs isolated from patients with either CD46 deficiency or with NLRP3 hyperactivity to determine that CD46 is also required for normal IFN-gamma secretion as well as killing activity in CTLs, whilst a canonical NLRP3 inflammasome is not required for these key functions. The CD46-deficient patient utilized in this study has a mutation in the CD46 gene that leads to reduced cell surface CD46 expression and a dysfunction in Th1 induction. The patient suffers from episodes of atypical hemolytic uremic syndrome (aHUS) and common variable immune deficiency (CVID) and recurrent infections.

2018-09-14 | GSE119913 | GEO

Transcriptome analysis of CD8+ T cells from healthy controls and patients wth CD46 deficiency

Project description:RNA-seq data from CD8+ T cells of healthy controls and patients with CD46-deficiency activated, or not, in vitro

2018-09-14 | GSE119918 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of CD46-KO/control vector, CD46-KO/CD46-CYT1 and CD46-KO/CD46-CYT2 EJ-1 cells’ Transcriptomes

Project description:CD46 is well known to be involved in diverse biological processes. Although several splice variants of CD46 have been identified, little is known about the contribution of alternative splicing to its tumorigenic functions. Here we found that exclusion of CD46 exon13 is significantly increased in bladder cancer samples. In bladder cancer cell lines, enforced expression of CD46-CYT2 (exon13-skipping isoform) induced cell growth and migration, and promoted tumorigenicity in a xenograft model. While enforced expression of CD46-CYT1 (exon13-containing isoform) attenuated tumorigenicity, representing an inverse phenotype of CD46-CYT2. We also used RNA sequencing to identify changes in gene expression after CD46-CYT1 or CD46-CYT2 overexpression and found KRT19 is a key CD46-CYT2 target gene. Furthermore, we applied interaction proteomics to identify exhaustively the complexes containing CYT1 or CYT2 domain in EJ-1 cells. 320 proteins were identified that interact with CYT1 or/and CYT2 domain, including some well-known CYT1 partners and most of them are new interactors. The new CYT2 partners’ translation machinery, RPL17 and EIF5A, were confirmed by coimmunoprecipitation experiments. We demonstrated that CD46-CYT2 enhances mRNA translation perhaps through an interaction with the translation machinery. Strikingly, the splicing factor SRSF1 is upregulated in bladder cancer and stimulates exclusion of exon13. Importantly, SRSF1 is highly correlated with CD46 exon13 exclusion in clinical bladder cancer samples. Taken together, our findings contribute to understanding the role of CD46 in bladder cancer development.

2019-12-31 | GSE117135 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of CD46-KO/control vector, CD46-KO/CD46-CYT1 and CD46-KO/CD46-CYT2 EJ-1 cells’ Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of CD46-KO/control vector, CD46-KO/CD46-CYT1 and CD46-KO/CD46-CYT2 EJ-1 cells’ Transcriptomes

| PRJNA481260 | ENA

Gene expression in T cells from CD46-deficient patients and matcherd healthy controls

Project description:Gene expression in T cells from CD46-deficient patients and matcherd healthy controls

| PRJNA490693 | ENA

Transcriptome analysis of CD8+ T cells from healthy controls and patients wth CD46 deficiency

Project description:Transcriptome analysis of CD8+ T cells from healthy controls and patients wth CD46 deficiency

| PRJNA490710 | ENA

CRISPR-Cas9 mediated editing of the CD46 gene in primary human B cells prior to their infection with Epstein-Barr virus (EBV) – analysis of CD46 transcripts after 24 hours

Project description:Adenoid B cells from anonymous human donors were isolated and nucleofected with RNP complexes targeting two loci within exon 2 of the CD46 gene, which encodes a cell surface protein. One hour after nucleofection, the same number of control cells (w/o-RNP) and CD46-RNP complex treated cells were infected with Epstein-Barr virus (strain 6008_B95-8) with a multiplicity of infection of 0.1. Newly transcribed RNAs were metabolically labeled with 4-thiouridine (4sU) for 60 min 23 hours after EBV infection. Twenty-four hours after the start of the experiment, 4sU-biotin-labeled, newly transcribed RNAs were thiol-specifically biotinylated and separated from unlabeled RNA using Streptavidin beads. RNA-seq experiments with the enriched RNA samples were performed to analyze the edited CD46 locus encompassing the RNP complex target sites. The experiment revealed that 24 hours after CRISPR-Cas9 mediated gene editing a substantial fraction of CD46 transcript contained indels and a larger deletion in between the two targets sites within exon 2 of CD46.

2020-10-18 | E-MTAB-9531 | biostudies-arrayexpress

Clostridioides difficile CD46

Project description:Clostridioides difficile CD46 Genome sequencing and assembly

| PRJNA85711 | ENA

Single-cell sequecing of LCMV-specific WT and HIF-1a-deficient CD8 T cells isolated from LCMV-Clone13 infected host mice

Project description:To determine the role of hypoxia-inducible factor 1 alpha (HIF-1a) in exhausted T cells, we crossed Hif1a-fl/fl Cd4-Cre mice to tdTomato+ P14 animals and adoptively co-transferred equal numbers of WT and HIF-1a-deficient P14 CD8+ T cells into chronically infected WT host mice. 21 days post infection, we retrieved GFP+ (WT) and tdTomato+ (HIF-1a-deficient) donor P14 T cells by FACS sorting and subjected CITE-seq antibody-barcoded WT and HIF-1a-deficient CD8+ P14 T cells to multiplexed scRNA sequencing analysis.

2023-09-22 | GSE213847 | GEO

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