Hyperoxia augments ER-stress-induced cell death independent of BiP loss. - sprookjes - yvandenbroek - TriplyDB

Hyperoxia augments ER-stress-induced cell death independent of BiP loss.

Hyperoxia augments ER-stress-induced cell death independent of BiP loss.

http://www.wikidata.org/entity/Q37441346

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DNA double-strand breaks activate ATM independent of mitochondrial dysfunction in A549 cells PKR-dependent CHOP induction limits hyperoxia-induced lung injury.Matrix protein CCN1 induced by bacterial DNA and CpG ODN limits lung inflammation and contributes to innate immune homeostasis The RNA surveillance protein SMG1 activates p53 in response to DNA double-strand breaks but not exogenously oxidized mRNA.Hyperoxia activates ATM independent from mitochondrial ROS and dysfunction.Endoplasmic reticulum stress mediating downregulated StAR and 3-beta-HSD and low plasma testosterone caused by hypoxia is attenuated by CPU86017-RS and nifedipine.Lung epithelial cell-derived extracellular vesicles activate macrophage-mediated inflammatory responses via ROCK1 pathway.Hyperoxia and interferon-γ-induced injury in developing lungs occur via cyclooxygenase-2 and the endoplasmic reticulum stress-dependent pathway.Engineers are from PDMS-land, Biologists are from Polystyrenia.Oxygen regulates molecular mechanisms of cancer progression and metastasis.Hyperoxia-induced activation of the integrated stress response in the newborn rat lung.Simple replica micromolding of biocompatible styrenic elastomers Developmental competence of bovine early embryos depends on the coupled response between oxidative and endoplasmic reticulum stress.Thermoplastic elastomer with advanced hydrophilization and bonding performances for rapid (30 s) and easy molding of microfluidic devices.

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Hyperoxia augments ER-stress-induced cell death independent of BiP loss.

http://www.wikidata.org/entity/Q37441346

description

article científic

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article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

@tr

scientific article published on 26 September 2009

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vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

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name

Hyperoxia augments ER-stress-induced cell death independent of BiP loss.

@en

Hyperoxia augments ER-stress-induced cell death independent of BiP loss.

@nl

type

label

Hyperoxia augments ER-stress-induced cell death independent of BiP loss.

@en

Hyperoxia augments ER-stress-induced cell death independent of BiP loss.

@nl

prefLabel

Hyperoxia augments ER-stress-induced cell death independent of BiP loss.

@en

Hyperoxia augments ER-stress-induced cell death independent of BiP loss.

@nl

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J.FREERADBIOMED.2009.09.022

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Free Radical Biology and Medicine

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Hyperoxia augments ER-stress-induced cell death independent of BiP loss.

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Jennifer S Gewandter

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Michael A O'Reilly

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Rhonda J Staversky

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P2860

Mammalian transcription factor ATF6 is synthesized as a transmembrane protein and activated by proteolysis in response to endoplasmic reticulum stress

XBP1 mRNA is induced by ATF6 and spliced by IRE1 in response to ER stress to produce a highly active transcription factor

Dimerization and release of molecular chaperone inhibition facilitate activation of eukaryotic initiation factor-2 kinase in response to endoplasmic reticulum stress

Coupling endoplasmic reticulum stress to the cell death program: role of the ER chaperone GRP78

Aging: a theory based on free radical and radiation chemistry

An essential dimer-forming subregion of the endoplasmic reticulum stress sensor Ire1.

Two regulatory steps of ER-stress sensor Ire1 involving its cluster formation and interaction with unfolded proteins.

IRE1 couples endoplasmic reticulum load to secretory capacity by processing the XBP-1 mRNA

ER stress regulation of ATF6 localization by dissociation of BiP/GRP78 binding and unmasking of Golgi localization signals

Knockdown of ERp57 increases BiP/GRP78 induction and protects against hyperoxia and tunicamycin-induced apoptosis.

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1742-1752

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10.1016/J.FREERADBIOMED.2009.09.022

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12

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