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Ablation of ER stress-linked kinase PERK in cancer cells elicits protective T cell immunity by paraptosis immunogenic cell death-induced Type-I IFN

ABSTRACT: C57BL6 wildtype mice were injected with B16F10 melanoma transduced with either untargeted sgRNA (Scramble) or PERK (EIF2AK3) knockout (KO) sgRNA. At day 17, tumors were harvested to isolate cKit+ (CD117) precursors via magnetic bead enrichment. These cKit expressing precursors were then sequenced.

ORGANISM(S): Mus musculus

PROVIDER: GSE206783 | GEO | 2022/07/28

REPOSITORIES: GEO

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AMPK activation enhances apoptotic priming and BCL2 dependence via PERK phosphorylation

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2015-09-01 | E-GEOD-49598 | biostudies-arrayexpress

ISR pathway activation signatures in MEFs: GCN2 and PERK

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PERK is a critical metabolic hub for immunosuppressive function in macrophages

Project description:Here we report that the Th2 cytokine IL-4 and the tumor microenvironment activated protein kinase RNA-like ER kinase (PERK) ER stress signaling cascade to promote immunosuppressive M2 activation and proliferation. Lacking PERK signaling impeded mitochondrial respiration and lipid oxidation critical for M2 macrophages. In addition, PERK activation mediated the upregulation of PSAT1 and serine biosynthesis via the downstream transcription factor ATF4.

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Project description:To identify the target genes of integrated stress reponse (ISR) in skeletal muscle, we have employed whole genome microarray expression in muscle specific Fv2E-PERK transgenic mice and C2C12 myotubes expressed in Fv2E-PERK. As a result, we identified that Fgf21 mRNA expression was commonly induced in skeletal muscle and C2C12.

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Project description:Disruptions of the endoplasmic reticulum (ER) that perturb protein folding cause ER stress and elicit an unfolded protein response (UPR) that involves translational and transcriptional changes in gene expression aimed at expanding the ER processing capacity and alleviating cellular injury. Three ER stress sensors PERK, ATF6, and IRE1 implement the UPR. PERK phosphorylation of eIF2 during ER stress represses protein synthesis, which prevents further influx of ER client proteins, along with preferential translation of ATF4, a transcription activator of the integrated stress response. In this study we show that the PERK/eIF2α~P/ATF4 pathway is required not only for translational control, but also activation of ATF6 and its target genes. The PERK pathway facilitates both the synthesis of ATF6 and trafficking of ATF6 from the ER to the Golgi for intramembrane proteolysis and activation of ATF6. As a consequence, liver-specific depletion of PERK significantly reduces both the translational and transcriptional phases of the UPR, leading to reduced protein chaperone expression, disruptions of lipid metabolism, and enhanced apoptosis. These findings show that the regulatory networks of the UPR are fully integrated, and helps explain the diverse pathologies associated with loss of PERK. 14 gene expression arrays, 3 WT control arrays; 3 lsPERK control arrays; 4 WT Treated arrays; 4 lsPERK treated arrays. Comparison of gene expression profiles for treated vs control in wildtype and knock-out.

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