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Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins [HotvsCold]

ABSTRACT: Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins [HotvsCold]

PROVIDER: PRJNA971503 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24503754.fastq.gz	Fastqsanger.gz
	SRR24503755.fastq.gz	Fastqsanger.gz
	SRR24503756.fastq.gz	Fastqsanger.gz
	SRR24503757.fastq.gz	Fastqsanger.gz
	SRR24503758.fastq.gz	Fastqsanger.gz

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Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins

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Project description:Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins [Liver]

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Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins [scRNAseq]

Project description:Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins [scRNAseq]

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Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins [Liver]

Project description:We sought to understand the mechanism by which hepatocytes coordinate immune surveillance

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Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins [HotvsCold]

Project description:To define changes in the liver that coordinate systemic inflammation and T cell surveillance, we performed RNA sequencing on livers of mice with T cellhigh and T celllow tumors.

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Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins

Project description:This SuperSeries is composed of the SubSeries listed below.

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Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins [scRNAseq]

Project description:We considered the possibility that STAT3 signaling specifically in hepatocytes may influence T cell surveillance in cancer

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Hepatocytes coordinate immune evasion in cancer via release of serum amyloid A proteins [Tumor]

Project description:We considered the possibility that STAT3 signaling specifically in hepatocytes may influence T cell surveillance in cancer

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Irisin reduces Amyloid-β by inducing the release of neprilysin from astrocytes following downregulation of ERK-STAT3 signaling

Project description:A pathological hallmark of Alzheimer’s disease (AD) is the deposition of amyloid-β protein (Aβ) in the brain. Physical exercise has been shown to reduce Aβ burden in various AD mouse models, but the underlying mechanisms have not been elucidated. Irisin, an exercise-induced hormone, is the secreted form of fibronectin-domain III containing 5 (FNDC5). Here, using a three-dimensional (3D) cell culture model of AD, we show that irisin significantly reduces Aβ pathology by increasing astrocytic release of the Aβ-degrading enzyme neprilysin (NEP). This is mediated by downregulation of ERK-STAT3 signaling. Finally, we show that integrin αV/β5 acts as the irisin receptor on astrocytes required for irisin-induced release of astrocytic NEP, leading to clearance of Aβ. Our findings reveal for the first time a cellular and molecular mechanism by which exercise-induced irisin attenuates Aβ pathology, suggesting a new target pathway for therapies aimed at the prevention and treatment of AD

2023-09-08 | GSE240161 | GEO

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