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Hemorrhage-induced NRF2 signaling in tumor-associated macrophages drives cancer growth, invasion, and immunotherapy resistance

ABSTRACT: Hemorrhage-induced NRF2 signaling in tumor-associated macrophages drives cancer growth, invasion, and immunotherapy resistance

PROVIDER: PRJNA996034 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25118716.fastq.gz	Fastqsanger.gz
	SRR25118717.fastq.gz	Fastqsanger.gz
	SRR25146892.fastq.gz	Fastqsanger.gz
	SRR25146893.fastq.gz	Fastqsanger.gz
	SRR25146894.fastq.gz	Fastqsanger.gz

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Hemorrhage-activated NRF2 in tumor-associated macrophages drives cancer growth, invasion, and immunotherapy resistance.

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Hemorrhage-induced NRF2 signaling in tumor-associated macrophages drives cancer growth, invasion, and immunotherapy resistance

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NRF2 supports non-small cell lung cancer growth independently of CBP/p300-enhanced glutathione synthesis

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Project description:Secondary injury causes death and dependence after spontaneous intracerebral haemorrhage (ICH). Having found that ICH is associated with activation of genes regulated by the transcription factor Nrf2, particularly in mononuclear myeloid cells (for example, monocyte-derived cells (MdC) and microglia), we sought to determine the importance of Nrf2 to mononuclear myeloid cell responses and their impact on ICH pathology. We used intrastriatal injection of collagenase to induce ICH in both wild-type mice, and knockout mice with Cx3cr1-Cre-mediated excision of Nrf2 (Nfe2l2) exon 5.

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Neutrophils after mouse subarachnoid hemorrhage

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Interleukin-22 immunotherapy modulates pulmonary gene expression evocative of enhanced tissue barrier and reduces bacterial systemic invasion during severe influenza

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