about
Inflammasome-dependent IL-1β release depends upon membrane permeabilisationFenamate NSAIDs inhibit the NLRP3 inflammasome and protect against Alzheimer's disease in rodent modelsThe NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory responseEfficient discovery of anti-inflammatory small-molecule combinations using evolutionary computingNeuronal injury induces the release of pro-interleukin-1beta from activated microglia in vitroInhibition of calpain blocks the phagosomal escape of Listeria monocytogenes.Inflammasomes as therapeutic targets for Alzheimer's disease.Dendritic cell IL-1α and IL-1β are polyubiquitinated and degraded by the proteasome.Extracellular ATP and P2X7 receptors in neurodegeneration.AIM2 and NLRC4 inflammasomes contribute with ASC to acute brain injury independently of NLRP3.Two zinc uptake systems contribute to the full virulence of Listeria monocytogenes during growth in vitro and in vivo.Inhibiting the Inflammasome: A Chemical Perspective.P2X7R activation drives distinct IL-1 responses in dendritic cells compared to macrophages.Obese mice exhibit an altered behavioural and inflammatory response to lipopolysaccharide.Molecular and Translational Classifications of DAMPs in Immunogenic Cell Death.Sphingosine regulates the NLRP3-inflammasome and IL-1β release from macrophages.Deubiquitinases regulate the activity of caspase-1 and interleukin-1β secretion via assembly of the inflammasomeMechanisms of regulation for interleukin-1beta in neurodegenerative disease.Pannexin-1-dependent caspase-1 activation and secretion of IL-1beta is regulated by zincDual functionality of interleukin-1 family cytokines: implications for anti-interleukin-1 therapyRegulation of interleukin-1 in acute brain injury.Understanding the mechanism of IL-1β secretionCaspase-1: is IL-1 just the tip of the ICEberg?The role of inflammation and interleukin-1 in acute cerebrovascular disease.Interleukin-1α and brain inflammation.Interleukin-1 as a pharmacological target in acute brain injury.Potassium efflux fires the canon: Potassium efflux as a common trigger for canonical and noncanonical NLRP3 pathways.Unconventional Pathways of Secretion Contribute to Inflammation.Acid-dependent Interleukin-1 (IL-1) Cleavage Limits Available Pro-IL-1β for Caspase-1 Cleavage.Novel perspectives on non-canonical inflammasome activation.Inflammasomes link vascular disease with neuroinflammation and brain disorders.Apoptosis-associated speck-like protein containing a CARD forms specks but does not activate caspase-1 in the absence of NLRP3 during macrophage swelling.Acidosis drives damage-associated molecular pattern (DAMP)-induced interleukin-1 secretion via a caspase-1-independent pathway.P2X7 receptor-dependent tuning of gut epithelial responses to infection.The dynamics and mechanisms of interleukin-1alpha and beta nuclear import.Zinc depletion regulates the processing and secretion of IL-1β.Caspase-1-dependent processing of pro-interleukin-1beta is cytosolic and precedes cell death.Release of interleukin-1α or interleukin-1β depends on mechanism of cell death.The structural integrity of the endoplasmic reticulum, and its possible regulation by inositol 1,3,4,5-tetrakisphosphate.Agonist-induced regulation of mitochondrial and endoplasmic reticulum motility.
P50
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P50
description
hulumtues
@sq
researcher
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wetenschapper
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հետազոտող
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name
David Brough
@ast
David Brough
@en
David Brough
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David Brough
@nl
David Brough
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type
label
David Brough
@ast
David Brough
@en
David Brough
@es
David Brough
@nl
David Brough
@sl
prefLabel
David Brough
@ast
David Brough
@en
David Brough
@es
David Brough
@nl
David Brough
@sl
P106
P21
P31
P496
0000-0002-2250-2381