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BLISTER safeguards the protein kinase activity of ER stress modulator IRE1A during plant growth and development in Arabidopsis thaliana

ABSTRACT: BLI tightly controls the protein kinase activity of IRE1A in plants,and IRE1A plays new roles in plant growth and development

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE124235 | GEO | 2019/11/01

REPOSITORIES: GEO

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BLISTER-regulated vegetative growth is dependent on the protein kinase domain of ER stress modulator IRE1A in Arabidopsis thaliana.

Project description: Not available

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BLISTER safeguards the protein kinase activity of ER stress modulator IRE1A during plant growth and development in Arabidopsis thaliana

Project description:BLISTER safeguards the protein kinase activity of ER stress modulator IRE1A during plant growth and development in Arabidopsis thaliana

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Expression data from IRE1a or XBP1 deficient mouse liver

Project description:IRE1a and XBP1 are key regulators of the unfolded protein response (UPR). XBP1 ablation causes profound hypolipidemia in mice, and triggers feedback activation of its upstream enzyme IRE1a, instigating regulated IRE1-dependent decay (RIDD), an mRNA degradation mechanism dependent on IRE1a's endoribonuclease activity. Comprehensive microarray analysis of XBP1 and/or IRE1a deficient liver identified genes involved in lipogenesis and lipoprotein metabolism as RIDD substrates, which might contribute to the suppression of plasma lipid levels by activated IRE1a. To identify RIDD substrate mRNAs and direct XBP1 targets in the liver, we performed a comprehensive comparative microarray analysis of three groups of RNA samples: WT and XBP1 deficient mice, WT and IRE1a deficient mice untreated or injected with tunicamycin, and XBP1 deficient mice injected with luciferase or IRE1a siRNA.

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BCL-2 modulates IRE1a activation to attenuate ER stress and pulmonary fibrosis

Project description:BCL-2 modulates IRE1a activation to attenuate ER stress and pulmonary fibrosis. Mice were treated with Bleomycin + Vehicle or Bleomycin + Navitoclax. Lungs were harvested 21 days after bleomycin injury followed by enzymatic digestion of the lungs to create single cell suspension and flow-sorting based isolation of total epithelial and stromal cells

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Expression data from primary hepatocytes knocking down or overexpressing IRE1a

Project description:The ER-resident protein kinase/endoribonuclease IRE1 is activated through trans-autophosphorylation in response to protein folding overload in the ER lumen and maintains ER homeostasis by triggering a key branch of the unfolded protein response. Here we show that mammalian IRE1a in liver cells is also phosphorylated by a kinase other than itself in response to metabolic stimuli. Glucagon stimulated protein kinase PKA, which in turn phosphorylated IRE1a at Ser724, a highly conserved site within the kinase activation domain. Blocking Ser724 phosphorylation impaired the ability of IRE1a to augment the upregulation by glucagon signaling of the expression of gluconeogenic genes. Moreover, hepatic IRE1a was highly phosphorylated at Ser724 by PKA in mice with obesity, and silencing hepatic IRE1a markedly reduced hyperglycemia and glucose intolerance. Hence, these results suggest that IRE1a integrates signals from both the ER lumen and the cytoplasm in the liver and is coupled to the glucagon signaling in the regulation of glucose metabolism. We used DNA microarray to analyze the transcriptomic change upon IRE1a overexpression or IRE1a depletion in primary hepatocytes, to study the changes related to IRE1a Primary hepatocytes were infected with the desired adenoviruses (Ad-EGFP, Ad-WT, Ad-S724A, Ad-shCON, Ad-shIRE1a#2) or treated with glucagon. Total cellular RNA was isolated with TRIzol (Invitrogen) and subjected to analysis by Affymetrix Mouse Genome 430 2.0 Arrays. Three experiments were independently conducted.

2011-08-30 | E-GEOD-31638 | biostudies-arrayexpress

Expression data from primary hepatocytes knocking down or overexpressing IRE1a

2011-08-31 | GSE31638 | GEO

Expression data from IRE1a or XBP1 deficient mouse liver

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SARS-CoV-2 diverges from other betacoronaviruses in only partially activating the IRE1a/XBP1 ER stress pathway in human lung-derived cells

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has killed over 6 million individuals worldwide and continues to spread in countries where vaccines are not yet widely available, or its citizens are hesitant to become vaccinated. Therefore, it is critical to unravel the molecular mechanisms that allow SARS-CoV-2 and other coronaviruses to infect and overtake the host machinery of human cells. Coronavirus replication triggers endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR), a key host cell pathway widely believed essential for viral replication. We examined the master UPR sensor IRE1a kinase/RNase and its downstream transcription factor effector XBP1s, which is processed through an IRE1a-mediated mRNA splicing event, in human lung-derived cells infected with betacoronaviruses. We found human respiratory coronavirus OC43 (HCoV-OC43), Middle East respiratory syndrome coronavirus (MERS-CoV), and murine coronavirus (MHV) all induce ER stress and strongly trigger the kinase and RNase activities of IRE1a as well as XBP1 splicing. In contrast, SARS-CoV-2 only partially activates IRE1a through autophosphorylation, but its RNase activity fails to splice XBP1. Moreover, while IRE1a was dispensable for replication in human cells for all coronaviruses tested, it was required for maximal expression of genes associated with several key cellular functions, including the interferon signaling pathway, during SARS-CoV-2 infection. Our data suggest that SARS-CoV-2 actively inhibits the RNase of autophosphorylated IRE1a, perhaps as a strategy to eliminate detection by the host immune system.

2022-07-20 | GSE193169 | GEO

Effect of the IRE1a-XBP1 pathway inhibition during T helper 2 differentiation

Project description:The purpose of the study was to examine the role of the IRE1a-XBP1 pathway during Th2 lymphocyte activation and differentiation. In vitro Th2 cells were treated with 4μ8c, a drug that specifically inhibits IRE1a endonuclease activity, and transcriptomes were compared.

2018-07-20 | E-MTAB-6894 | biostudies-arrayexpress

Effect of IRE1a and XBP1 knockdown on gene expression in primary mouse keratinocytes expressing an HRas oncogene

Project description:IRE1a is a critical modulator of the unfolded protein response. Its RNAse activity generates the mature transcript for the XBP1 transcription factor and also degrades other ER associated mRNAs in a process termed Regulated IRE1a Dependent mRNA Decay or RIDD. To determine if IRE1a is critical in the response to oncogenic Ras we used ShRNA to knockdown Ire1a or Xbp1 in primary mouse epidermal keratinocytes transduced with a v-HRAS retrovirus.

2017-06-01 | GSE70899 | GEO

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