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Mus musculus

ABSTRACT: De novo epigenetic programs inhibit PD-1 blockade-mediated T-cell rejuvenation [WGBS]

PROVIDER: PRJNA388487 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5629710.fastq.gz	Fastqsanger.gz
	SRR5629710_1.fastq.gz	Fastqsanger.gz
	SRR5629710_2.fastq.gz	Fastqsanger.gz
	SRR5629711.fastq.gz	Fastqsanger.gz
	SRR5629711_1.fastq.gz	Fastqsanger.gz

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De novo epigenetic programs inhibit PD-1 blockade-mediated T-cell rejuvenation

Project description:De novo epigenetic programs inhibit PD-1 blockade-mediated T-cell rejuvenation

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De novo epigenetic programs inhibit PD-1 blockade-mediated T-cell rejuvenation [WGBS]

Project description:De novo DNA methylation establishes T cell exhaustion and inhibits PD-1 blockade-mediated T-cell rejuvenation.

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De novo epigenetic programs inhibit PD-1 blockade-mediated T-cell rejuvenation [expression]

Project description:De novo DNA methylation establishes T cell exhaustion and inhibits PD-1 blockade-mediated T-cell rejuvenation. Expression profiling of chronically stimulated WT and Dnmt3a cKO antigen-specific CD8 T cells.

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Tumor-Infiltrating Myeloid Cells Confer de novo Resistance to PD-L1 Blockade through EMT-stromal and Tgf-beta Dependent Mechanisms

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Targeting PURPL RNA Enabled Rejuvenation of Senescence Cells via Epigenetic Reprogramming

Project description:Cellular senescence is a fundamental driver of ageing and age-related diseases, characterized by irreversible growth arrest and profound epigenetic alterations. While long non-coding RNAs (lncRNAs) have emerged as key regulators of senescence, their potential for senescent cell rejuvenation remains unexplored. Here, we identify the ageing-associated lncRNA PURPL as an epigenetic regulator that controls cellular rejuvenation through H3K9me3-mediated transcriptional silencing. CRISPRi-mediated PURPL depletion produces striking rejuvenation effects, resulting in restored youthful cell morphology, as well as suppression of senescence markers such as p21 and SA-β-gal. Conversely, PURPL overexpression accelerates cellular senescence, recapitulating the transcriptional and phenotypic hallmarks of ageing. Mechanistically, nuclear-localized PURPL regulates H3K9me3 deposition at 411 genomic loci including SERPINE1 (PAI-1) and EGR1, which are key senescence drivers. PURPL-mediated H3K9me3 loss at these loci derepresses their transcription, establishing a pro-senescence gene expression program. These findings reveal that PURPL is an epigenetic modulator of senescence and highlight its potential as a therapeutic target for age-related pathologies.

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Project description:Convergence of aging- and rejuvenation-related epigenetic alterations on PRC2 targets [WGBS]

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