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PKCα-LSD1-NF-κB Signaling Cascade Is Crucial for Epigenetic Control of the Inflammatory Response

ABSTRACT: PKCα-LSD1-NF-κB Signaling Cascade Is Crucial for Epigenetic Control of the Inflammatory Response

PROVIDER: PRJNA422239 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5713220_1.fastq.gz	Fastqsanger.gz
	SRR5713220_2.fastq.gz	Fastqsanger.gz
	SRR5713221_1.fastq.gz	Fastqsanger.gz
	SRR5713221_2.fastq.gz	Fastqsanger.gz
	SRR5713222_1.fastq.gz	Fastqsanger.gz

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PKCα-LSD1-NF-κB Signaling Cascade Is Crucial for Epigenetic Control of the Inflammatory Response [RNA-Seq]

Project description:The inflammatory response mediated by NF-κB signaling is essential for host defense against pathogens. Although the components and regulatory mechanism of NF-κB signaling have been well-studied, molecular basis for the epigenetic regulation of the inflammatory response is poorly understood. Here, we identify a new signaling axis of PKCα- LSD1-NF-κB p65 which is critical for activation and amplification of the inflammatory response and triggering systemic inflammatory diseases. In response to excessive inflammatory stimuli, PKCα translocates to the nucleus and phosphorylates LSD1. Phosphorylation of LSD1 is required for its interaction with p65 and facilitates demethylation of p65 leading to enhanced protein stability. Genome-wide analysis reveals a critical role of LPS-induced LSD1 phosphorylation in the transcriptional activation of NF-κB target genes. Together, we demonstrate that PKCα-LSD1-NF-κB signaling cascade is crucial for epigenetic control of the inflammatory response.

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PKCα-LSD1-NF-κB Signaling Cascade Is Crucial for Epigenetic Control of the Inflammatory Response [ChIP-Seq]

Project description:PKCα-LSD1-NF-κB Signaling Cascade Is Crucial for Epigenetic Control of the Inflammatory Response [ChIP-Seq]

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PKCα-LSD1-NF-κB Signaling Cascade Is Crucial for Epigenetic Control of the Inflammatory Response

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

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Project description:PKCα-LSD1-NF-κB Signaling Cascade Is Crucial for Epigenetic Control of the Inflammatory Response [RNA-Seq]

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Project description:Despite remarkable achievements, majority of hepatocellular carcinoma (HCC) patients fail to respond to anti-PD1 therapy. Here, we showed that ZFP64 was frequently upregulated in HCC tissues of anti-PD1 resistance patients. Elevated ZFP64 levels triggered tumor progression and induced an immunosuppressive microenvironment. Mechanistically, ZFP64 transcriptionally activated colony-stimulating factor 1 (CSF1) by directly binding to its promoter, and secreted CSF1 driving the shift of macrophages into an alternatively activated phenotype. Importantly, the PKCα was revealed to phosphorylate ZFP64 at S226, resulting in its nuclear translocation to transcribe the CSF1 gene. Particularly, we proposed firstly that the PKCα/ZFP64/CSF1 axis was a critical pathway in fostering immune evasion and anti-PD1 tolerance and inhibiting this axis with lenvatinib or Gö6976 surmounted the anti-PD1 resistance in HCC. Our study indicates that the ZFP64 is an emerging indicator in predicting anti-PD1 efficacy, and reveals the PKCα/ZFP64/CSF1 axis is a suitable target for anti-PD1 combination therapy in HCC.

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