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Transcription profiling of mouse PERK knockouts vs. wikd type

ABSTRACT: to study the proliferation of PERK knockout mice islets. The major changes are the proliferation genes Experiment Overall Design: 2days after birth, Experiment Overall Design: Collagenase P digestion Experiment Overall Design: cRNA label with Ambion kit Experiment Overall Design: Hybridization with Affymetrix mouse 430A chip

ORGANISM(S): Mus musculus

SUBMITTER: YULIN LI

PROVIDER: E-GEOD-6193 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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PERK EIF2AK3 control of pancreatic beta cell differentiation and proliferation is required for postnatal glucose homeostasis.

Zhang Wei W Feng Daorong D Li Yulin Y Iida Kaori K McGrath Barbara B Cavener Douglas R DR

Cell metabolism 20061201 6

Mutations in PERK (EIF2AK3) result in permanent neonatal diabetes as well as several other anomalies that underlie the human Wolcott-Rallison syndrome, and these anomalies are mirrored in Perk knockout mice. To identify the cause of diabetes in PERK-deficient mice, we generated a series of tissue- and cell-specific knockouts of the Perk gene and performed a developmental analysis of the progression to overt diabetes. We discovered that PERK is specifically required in the insulin-secreting beta ...[more]

PMID: 17141632

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Transcription profiling of mouse PERK mutant vs. wild type

Project description:Molecular characterization of PERK's role in the mouse exocrine pancreas. Postnatal days 16, 19 and 32 were examined. Postnatal day 16 represents a stage immediately prior to severe cytological changes in the exPKO mice. Postnatal day 19 represents the initial stage of severe phenotypes in the exPKO mice. Postnatal day 32 represents the middle stage of severe phenotypes (about 2 wks from the initiation) in the exPKO mice. Experiment Overall Design: Comparison between the two genotypes (Perk mutant vs. wild-type) at postnatal days 16, 19 and 32.

2008-06-13 | E-GEOD-4422 | biostudies-arrayexpress

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

Islet microarray on 2 days PERK wild type and knockout mice

Project description:to study the proliferation of PERK knockout mice islets. The major changes are the proliferation genes Keywords: cDNA microarray on genetically modified mouse islets

2006-10-30 | GSE6193 | 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) stress signaling cascade to promote immunosuppressive M2 activation and proliferation. PERK activation mediated the upregulation of PSAT1 and serine biosynthesis via the downstream transcription factor ATF4. We found that Increased serine biosynthesis could result in enhanced mitochondrial function and α-ketoglutarate (α-KG) production required for JMJD3-dependent epigenetic modification.

2022-01-01 | GSE183287 | GEO

Investigating proteome remodeling as a function of mammalian cell size

Project description:Investigating proteome remodeling as a function of mammalian cell size Experiment design: Condition1: RPE1 cells treated with palbociclib (2days) Condition 2: RPE1 cells treated with palbociclib (6days) Condition 3: RPE1 cells treated with palbociclib (6days) +Torin1 Condition 4: RPE1 cells treated with palbociclib (6days) contact inhibited

2024-01-26 | PXD034934 | Pride

ISR target genes revealed by comprehensive microarray network study using Perk -/-, Atf4 -/-, eIF2a S51A mutant, Fv2E-PERK

Project description:To identify the target genes of integrated stress reponse (ISR), we have employed whole genome microarray expression in MEF cells. ISR gene setimation under ER stress condition using Perk -/-, Atf4 -/-, eIF2a S51A mutant, Fv2E-PERK MEF cells

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

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.

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Targeting NLRP3 inhibits AML progression by inducing PERK/eIF2-mediated apoptosis

Project description:Hyperactivation of the NLRP3 inflammasome has been linked to disease progression in acute myeloid leukemia (AML). However, the precise mechanisms behind this pathology remain elusive. Here, we highlight not only a significant correlation between elevated NLRP3 expression and diminished overall survival in AML patients, but also a potential pathomechanism. We show that genetic deletion and pharmacological inhibition of NLRP3 leads to a reduction in AML cell survival by triggering apoptosis. Additionally, our proteomic analyses revealed NLRP3-dependent alterations in protein translation, substantiated by increased eIF2α phosphorylation in NLRP3-deficient AML cells. Furthermore, we show that inhibition of the eIF2α kinase PERK mitigates eIF2α phosphorylation and decreases apoptosis by reducing the expression of pro-apoptotic Bcl-2 family members to levels comparable to those of wild-type cells. Substantiating these observations, we found that deleting NLRP3 in engrafted AML cells led to reduced splenomegaly and AML cell infiltration into organs in mice. Taken together, our findings demonstrate that blocking NLRP3 induces apoptosis via PERK/eIF2, revealing a promising avenue for therapeutic intervention in AML.

2024-08-14 | PXD047745 | Pride

The PERK signaling controls myoblasts differentiation by regulating microRNA networks

Project description:By using small RNA-seq, we report microRNA profilings from Perk knockdown C2C12 cells, differentiated C2C12 cells, Atf4 overexpressed C2C12 cells, Perk knockdown P19 cells and negative control.

2021-03-01 | GSE167878 | GEO

ISR target genes in WAT and BAT of mAP::Fv2E-PERK

Project description:To identify the target genes of integrated stress reponse (ISR) in WAT and BAT, we have employed whole genome microarray expression in WAT and BAT specific Fv2E-PERK transgenic mice. The mAP::Fv2E-PERK transgenic mice were injected by AP20187 or mock.

2015-08-05 | E-GEOD-49645 | biostudies-arrayexpress

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