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Expression data of wild-type and perforin-knockout CAR-T cell

ABSTRACT: Expression data of wild-type and perforin-knockout CAR-T cell

PROVIDER: PRJNA541957 | ENA |

REPOSITORIES: ENA

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Expression data of wild-type and perforin-knockout CAR-T cell

Project description:Murine chimeric antigen receptor transduced T cells (CAR-T cells) deficient in perforin recapitulate hemophagocytic lymphohistiocytosis (HLH)-like toxicities occuring in human CAR-T recipients. We used microarray to describe gene expression profiles of wild-type and perforin-deficient CAR-T cells.

2020-10-07 | GSE130929 | GEO

Expression data from CAR knockout mouse E10.5 embryos

Project description:Gene expression analysis of whole heart samples obtained from CAR wild type and knockout mouse E10.5 embryos. We used the microarray to detect any gene expression changes in the E10.5 embronic heart due to the global deletion of CAR.

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Glycosylation landscape of CAR-T in AAVS1 and SPPL3 knockout

Project description:In this study, we delved into deciphering the glycosylation patterns and precise localization of glycosylation sites within CAR-T proteins. Specifically, we focused on samples derived from human T cells that underwent gene knockout of AAVS1 and SPPL3, two critical genes that could potentially influence CAR-T function. To ensure accuracy and precision, we employed optimal tribrid orbitrap mass spectrometry settings for glycosylation landscapes of the CAR-T proteins. By analyzing these data, we aimed to gain a deeper understanding of how AAVS1 and SPPL3 knockout impacted the glycosylation profiles and ultimately the function and efficacy of CAR-T cells in immunotherapy applications.

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Genome-wide Analysis of Human Constitutive Androstane Receptor (CAR) Transcriptome in Wild-type and CAR-knockout HepaRG cells

Project description:The constitutive androstane receptor (CAR, NR1I3) modulates the transcription of numerous genes involving drug metabolism, energy homeostasis, and cell proliferation. Most functions of CAR however were defined from animal studies. Given the known species difference of CAR and the significant cross-talk between CAR and the pregnane X receptor (PXR), it is extremely difficult to decipher the exact role of human CAR (hCAR) in gene regulation, relying predominantly on pharmacological manipulations. Here, utilizing a newly generated hCAR-knockout (KO) HepaRG cell line, we carried out RNA-seq analysis of the global transcriptomes in wild-type (WT) and hCAR-KO HepaRG cells treated with CITCO, a selective hCAR agonist, phenobarbital (PB), a dual activator of hCAR and hPXR, or vehicle control. Real-time PCR assays in separate experiments were used to validate RNA-seq findings. Our results indicate that genes encoding drug-metabolizing enzymes are among the main clusters altered by both CITCO and PB. Specifically, CITCO significantly changed the expression of 135 genes in an hCAR-dependent manner, while PB altered the expression of 227 genes in WT cells of which 94 were simultaneously modulated in both cell lines reflecting the dual effects of PB on hCAR/PXR. Notably, we found that many genes promoting cell proliferation and tumorigenesis were up-regulated in hCAR-KO cells, suggesting that hCAR may play an important role in cell growth that differs from mouse CAR. Together, our results reveal both novel and known targets of hCAR and support the role of hCAR in maintaining the homeostasis of metabolism and cell proliferation in the liver.

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E. Coli Nissle wild type versus knockout strain

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Expression data from CAR knockout mouse E10.5 embryos

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Project description:Wild type and AQP8 Knockout proteomes

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Microarray analysis of genes activated by mouse CAR and human CAR in vivo.

Project description:This dataset is a four-ligand x three-genotype Affymetrix microarray analysis of the regulation of liver genes in the mouse by the constitutive androstane receptor (CAR). 24 female mice of mixed background (C57BL/6x129Sv) were divided into three groups: wild-type (contains only mouse CAR; mCAR), CAR.KO = knockout mice (mice ablated for mCAR gene; mCAR -/-), and CAR.AH= contains human CAR transgene under the control of the mouse albumin promoter in the mCAR -/- background. Each of the three groups underwent four different treatment regimens: CO = corn oil vehicle control, PB = phenobarbitol (100 mg/kg/day), an anti-convulsant agent which can translocate both mCAR and hCAR into the nucleus to turn on target gene expression, TC = TCPOBOP, a potent non-metabolized ligand of mCAR (3 mg/kg), CITCO = a hCAR specific ligand (30 mg/kg/day). Two mice were used per treatment group and each mouse RNA was used for one chip.

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Project description:This study searched for cell-type specific effectors of endocytic escape in dendritic cells and identified a pore-forming protein, perforin-2 (encoded by Mpeg1), as a dedicated effector exclusive to cross-presenting cells. Whole cell proteomics identified differences in the abundance of tryptic and semi-tryptic (cleaved) perforin-2 peptides between control MutuDCs and cells treated with BafA, CpG or with knockout of asparagine endopeptidase (AEP). This revealed how perforin-2 undergoes proteolytic cleavage releasing its pore forming domain into the organellar lumen.

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