The Inflammasome and Autoinflammatory Syndromes.
San Diego, United States. In Annu Rev Pathol, 19 Dec 2014
We discuss our understanding of how inflammasomes assemble to trigger caspase-1 activation and subsequent cytokine release, describe how genetic mutations in inflammasome-related genes lead to autoinflammatory syndromes, and review the contribution of inflammasome activation to various pathologies arising from metabolic dysfunction.
A clear and present danger: inflammasomes DAMPing down disorders of pregnancy.
Derby, United Kingdom. In Hum Reprod Update, 17 Dec 2014
Inflammasomes are unique, intracellular, multiprotein assemblies that enable caspase-1 mediated proteolytic processing of the proinflammatory cytokine interleukin-1β, levels of which are elevated in some forms of preterm birth and maternal metabolic disorders.
Role of inflammasome activation in development and exacerbation of asthma.
Puch'ŏn, South Korea. In Asia Pac Allergy, Oct 2014
In addition to caspase-1 activation, proteinase 3 and other protease from activated neutrophils directly cleave pro-IL-1β and pro-IL-18 to IL-1β and IL-18, which contribute to the phenotype of subsequent adaptive immune responses without inflammasome activation.
To develop with or without the prion protein.
Jouy-le-Moutier, France. In Front Cell Dev Biol, Dec 2013
The deletion of the cellular form of the prion protein (PrP(C)) in mouse, goat, and cattle has no drastic phenotypic consequence.
Prions in Variably Protease-Sensitive Prionopathy: An Update.
More papers using
Cleveland, United States. In Pathogens, 2012
UNLABELLED: Human prion diseases, including sporadic, familial, and acquired forms such as Creutzfeldt-Jakob disease (CJD), are caused by prions in which an abnormal prion protein (PrPSc) derived from its normal cellular isoform (PrPC) is the only known component.