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Ku70/HP1g are presented at the KCl induced acutely activated enhancers [ChIP-seq]

ABSTRACT: Ku70/HP1g are presented at the KCl induced acutely activated enhancers [ChIP-seq]

PROVIDER: PRJNA770274 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16290005_1.fastq.gz	Fastqsanger.gz
	SRR16290005_2.fastq.gz	Fastqsanger.gz
	SRR16290006_1.fastq.gz	Fastqsanger.gz
	SRR16290006_2.fastq.gz	Fastqsanger.gz
	SRR16290007_1.fastq.gz	Fastqsanger.gz

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Ku70/HP1g are presented at the KCl induced acutely activated enhancers [ChIP-seq]

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Project description:Affinity purification coupled to mass spectrometry is often used as a complementary technique to BioID experiments, and the data presented here complements another project. To infer processes involving Ku70, we used AP-MS to identify candidate proteins that may interact with Ku70 and compared these results to those acquired using BioID with Ku70.

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Genome-wide mapping of Cbx3/HP1g deposition in wild-type CD8+ effector T cells

Project description:We report the application of Illumina Hi-Seq sequencing technology for high-throughput profiling of Cbx3/HP1g deposition in mammalian CD8+ effector T cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, genome-wide chromatin-state maps of mouse wt CD8+ effector T cells were generated. We find that Cbx3/HP1g negatively regulates the germinal center and high-affinity antibody responses in a CD8+ T-cell-dependent manner. CD8-restricted deletion of Cbx3/HP1g confers hightened effector and persistence capacity on CD8+ effector T cells. As a result, Cbx3/HP1g-deficient CD8+ effector T cells can efficiently control solid tumor growth in vairious mouse models (melanoma, ovarian and neuroblstoma).

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