about
Strain-dependent activation of NF-kappaB in the airway epithelium and its role in allergic airway inflammationRedox-based regulation of apoptosis: S-glutathionylation as a regulatory mechanism to control cell deathAbsence of c-Jun NH2-terminal kinase 1 protects against house dust mite-induced pulmonary remodeling but not airway hyperresponsiveness and inflammation.The glutaredoxin/S-glutathionylation axis regulates interleukin-17A-induced proinflammatory responses in lung epithelial cells in association with S-glutathionylation of nuclear factor κB family proteins.Nitric oxide represses inhibitory kappaB kinase through S-nitrosylationReactive nitrogen species-induced cell death requires Fas-dependent activation of c-Jun N-terminal kinaseCigarette smoke targets glutaredoxin 1, increasing s-glutathionylation and epithelial cell death.Induction of a mesenchymal expression program in lung epithelial cells by wingless protein (Wnt)/β-catenin requires the presence of c-Jun N-terminal kinase-1 (JNK1).In situ analysis of protein S-glutathionylation in lung tissue using glutaredoxin-1-catalyzed cysteine derivatization.Glutaredoxin-1 attenuates S-glutathionylation of the death receptor fas and decreases resolution of Pseudomonas aeruginosa pneumonia.Regulation of apoptosis through cysteine oxidation: implications for fibrotic lung disease.In situ detection of S-glutathionylated proteins following glutaredoxin-1 catalyzed cysteine derivatization.Nuclear factor-kappaB activation in airway epithelium induces inflammation and hyperresponsiveness.c-Jun N-terminal kinase 1 promotes transforming growth factor-β1-induced epithelial-to-mesenchymal transition via control of linker phosphorylation and transcriptional activity of Smad3.Distinct functions of airway epithelial nuclear factor-kappaB activity regulate nitrogen dioxide-induced acute lung injury.
P50
Q28393042-05B3034D-FFE6-4D93-A8D4-DB075EE052B4Q28397611-39B08269-6270-4F08-BDAD-0D8F8C8AE724Q33568654-C4170C7C-E3F8-467B-AF67-C0AFC4790C36Q33954291-6B1FE33E-3188-433A-BEB8-6160C5D77882Q34830350-CC34A7E3-D4D7-4D8A-9F29-0E3BEE84EE3BQ35663860-9786DB33-935D-49BB-BD64-63C4A2B8001AQ35684883-DE430929-03A7-454B-9E7E-BE9FC7A9E79FQ36370180-BE900522-79B6-4116-9E58-55159AEEE192Q37257106-D3DD77BB-76FA-4A51-8F88-25C8B4A3FBB9Q37688517-23D76C41-5291-4558-87E8-26B6F60B6BB5Q37780586-2564FD9D-4DC0-48C8-85A9-6D44E1ADC0E5Q40309074-0B6CB7D8-BAE5-4B7A-8569-7514CB922CF0Q41923388-48246DC5-6813-4AE5-B3B4-2D2D5AB12180Q42066518-4CA50FAF-C759-4FF2-96C3-B71B9781721FQ42412449-82321D4F-7020-40DB-8555-A1F251315EE8
P50
description
researcher ORCID ID = 0000-0002-6530-449X
@en
wetenschapper
@nl
name
Amy S Guala
@ast
Amy S Guala
@en
Amy S Guala
@nl
type
label
Amy S Guala
@ast
Amy S Guala
@en
Amy S Guala
@nl
prefLabel
Amy S Guala
@ast
Amy S Guala
@en
Amy S Guala
@nl
P106
P31
P496
0000-0002-6530-449X