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Gene expression profiles of wild-type and PERK-deficient cells during activation of OXPHOS

ABSTRACT: Gene expression profiles of wild-type and PERK-deficient cells during activation of OXPHOS

PROVIDER: PRJNA453130 | ENA |

REPOSITORIES: ENA

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Gene expression profiles of wild-type and PERK-deficient cells during activation of OXPHOS

Project description:Intracellular ATP is mainly produced by the glycolysis pathway in culture cells incubated with high-glucose medium, whereas ATP production is switched to the OXPHOS pathway by culturing with the no-glucose medium. To elucidate the potential function of PERK during activation of OXPHOS pathway, we perfomed RNA-sequencing analayais using wild-type and PERK-deficient HEK293 cells.

2020-02-03 | GSE113572 | GEO

Gene expression profiles of control or PERK siRNA-transfected brown adipocyte during the differentiation

Project description:The area of mitochondria in differentiated brown adipocytes is dramatically increased compared with that in brown pre-adipocytes. The ATP production is switched from the glycolysis pathway to the OXPHOS pathway during brown adipocyte differentiation. Endoplasmic reticulum (ER) is surrounded by mitochondria and the area of contact sites between mitochondria and the ER is increased. ER stress sensor PERK was phosphorylated during differentiation. To elucidate the mitochondria-ER crosstalk signaling mediated by PERK, RNA-sequencing analysis was performed using control siRNA- or PERK siRNA-transfected brown adipocytes.

2020-02-03 | GSE132598 | GEO

ISR pathway activation signatures in MEFs: GCN2 and PERK

Project description:In response to different cellular stressors, the ISR kinases, PERK, PKR, HRI and GCN2, activate downstream transcriptional programs. While the core ISR transcription program is well characterized, markers that are specific to each individual ISR kinase activation pathway are not known. To identify markers that are induced by PERK or GCN2, but not the other ISR kinases, we subjected WT, GCN2-/-, and PERK-/- MEFs to amino acid starvation (RPMI 1640 SILAC -Lys -Arg) or Thapsigargin (200nM) treatment for 6 hours to activate the GCN2 and PERK pathways, respectively and performed RNA sequencing.

2022-07-01 | GSE179559 | GEO

The eIF2 kinase PERK and the integrated stress response facilitate activation of ATF6 during endoplasmic reticulum stress

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.

2012-01-20 | E-GEOD-29929 | biostudies-arrayexpress

ISR pathway activation signatures in MEFs: GCN2 and PERK

Project description:ISR pathway activation signatures in MEFs: GCN2 and PERK

| PRJNA744201 | ENA

Pharmacologic Activation of a Compensatory Integrated Stress Response Kinase Promotes Adaptive Mitochondrial Remodeling in Perk-deficient Cells

Project description:mRNA sequencing of WT or PERK-/- MEFs treated with the ISR activating compounds BtdCPU, Halofuginone, and Thapsigargin.

2023-09-09 | GSE227134 | GEO

The eIF2 kinase PERK and the integrated stress response facilitate activation of ATF6 during endoplasmic reticulum stress

2012-01-20 | GSE29929 | GEO

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.

2022-01-01 | GSE165836 | GEO

Comparison of gene expression profiles of hearts in nulloparous (NP) or postpartum (PP) PERK wild type (flx) or PERK cardiac-specific knockout (cko) mice.

Project description:Recently, it is reported that multiple signaling pathways are involved with the pathogenesis of PPCM. Here, we show that PERK kockout affect these pathways in postpartum period.

2021-03-10 | GSE168536 | GEO

Comparison of gene expression profiles in hearts exposed to pressure overload (PO) with or without sildenafil treatment in PERK wild type (flx) or PERK cardiac-specific knockout 8cko) mice.

Project description:Recently, it is reported that sildenafil suppresses maturation of PO-induced miRNAs. However, the mechanism of how sildenafil coupled NO-cGMP-PKG signaling affects this maturation was not unraveled. Here, we show that PERK-mediated suppression of miRNAs by sildenafil is vital to keep mitochondrial homeostasis, using cardiac-specific PERK knockout (cko) mice.

2020-07-10 | GSE154081 | GEO

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