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Releasing the mitochondrial respiration brake MCJ/DnaJC15 enhances CD8 CAR-T cell therapy efficacy

ABSTRACT: Releasing the mitochondrial respiration brake MCJ/DnaJC15 enhances CD8 CAR-T cell therapy efficacy

PROVIDER: PRJNA1096360 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28560201_1.fastq.gz	Fastqsanger.gz
	SRR28560201_2.fastq.gz	Fastqsanger.gz
	SRR28560202_1.fastq.gz	Fastqsanger.gz
	SRR28560202_2.fastq.gz	Fastqsanger.gz
	SRR28560203_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Releasing the mitochondrial respiration brake MCJ/DnaJC15 enhances CD8 CAR-T cell therapy efficacy

Project description:Metabolism of chimeric antigen receptor (CAR) T cells is emerging as an important area to improve CAR-T cell therapy in cancer treatment. Mitochondrial respiration is essential for survival and function of CAR-T cells, but developing strategies to specifically enhance mitochondrial respiration has been challenging. Here we identify MCJ/DnaJC15, an endogenous negative regulator of mitochondrial Complex I, as a metabolic target to enhance mitochondrial respiration in CD8 CAR-T cells. Loss of MCJ in CD8 CAR-T cells increases their in vitro and in vivo efficacy against mouse B cell leukemias. MCJ deficiency in TCR- specific CD8 cells also increases their efficacy against solid tumors in vivo. Furthermore, we reveal that human CD8 cells express MCJ and that silencing MCJ expression increases mitochondrial metabolism and anti-tumor activity of human CAR-T cells. Thus, we demonstrate the unique therapeutic potential of targeting MCJ to enhance the metabolism and efficacy of adoptive T cell therapies.

2024-05-02 | GSE263259 | GEO

Absence of MCJ/DnaJC15 promotes brown adipose tissue thermogenesis

Project description:Obesity poses a global health challenge, demanding a deeper understanding of adipose tissue (AT) and its mitochondria. This study describes the role of the mitochondrial protein Methylation-controlled J protein (MCJ/DnaJC15) in orchestrating brown adipose tissue (BAT) thermogenesis. Here we show how MCJ expression decreases during obesity, as evident in human and mouse adipose tissue samples. MCJKO mice, even without UCP1, a fundamental thermogenic protein, exhibit elevated BAT thermogenesis. Electron microscopy unveils changes in mitochondrial morphology resembling BAT activation. Proteomic analysis confirms these findings and suggests involvement of the eIF2α mediated stress response. The pivotal role of eIF2α is scrutinized by in vivo CRISPR deletion of eIF2α in MCJKO mice, abrogating thermogenesis. These findings uncover the importance of MCJ as a regulator of BAT thermogenesis, presenting it as a promising target for obesity therapy.

2024-11-13 | PXD057026 | Pride

Enterococcus faecalis strain:MCJ

Project description:Enterococcus faecalis strain:MCJ Genome sequencing

| PRJNA1184011 | ENA

MCJ deficient mice gut metagenome

Project description:MCJ deficient mice gut metagenome

| PRJEB19385 | ENA

Histone Deacetylase 3 is an Epigenomic Brake in Macropahge Alternative Activation

Project description:This SuperSeries is composed of the following subset Series: GSE33596: Histone Deacetylase 3 is an Epigenomic Brake in Macrophage Alternative Activation (ChIP-Seq) GSE33608: Histone Deacetylase 3 is an Epigenomic Brake in Macrophage Alternative Activation (microarray) Refer to individual Series

2011-11-10 | E-GEOD-33609 | biostudies-arrayexpress

Dysbiosis MCJ colitis mice

Project description:Dysbiosis plus DSS induced colitis in MCJ-KO mice model

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Chronic model of ulcerative colitis with MCJ deficient mice

Project description:MCJ defiency chronic model of UC

| PRJEB44741 | ENA

MCJ-KO microbiota transplantation to GF mice and DSS-induced colitis

Project description:GF colonization with MCJ-KO

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WAS enhance organohalides respiration

Project description:WAS enhance organohalides respiration

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Bulk mRNA Seq CAR.CCR7 vs. CAR

Project description:The study aimed to elucidate the transcriptional changes introduced by genetic engineering of CAR T cells to stably express the homeostatic chemokine receptor CCR7. In vitro killing assays hinted to a higher cytolytic capacity that could be tied to an altered cytoskeletal rearrangement. Human CAR and CAR.CCR7 T cells were generated by retroviral transduction and enriched by FACS at the end of the expansion phase (day 10), either without or with a previous over-night co-culture with target Jeko1 tumor cells that express the CAR target antigen CXCR5. Enriched cells were immediately processed for bulk mRNA Seq

2023-06-30 | E-MTAB-12778 | biostudies-arrayexpress

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