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Cytochalasin B triggers a novel pertussis toxin sensitive pathway in TNF-alpha primed neutrophils
Authors:Johan?Bylund,Sara?Pellmé,Huamei?Fu,Ulf-Henrik?Mellqvist,Kristoffer?Hellstrand,Anna?Karlsson,Claes?Dahlgren  author-information"  >  author-information__contact u-icon-before"  >  mailto:Claes.Dahlgren@microbio.gu.se"   title="  Claes.Dahlgren@microbio.gu.se"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author
Affiliation:1.Department of Rheumatology and Inflammation Research,University of G?teborg,G?teborg,Sweden;2.Department of Paediatrics,University of British Columbia, BC Research Institute for Children's and Woman's Health,Vancouver,Canada;3.Department of Hematology,University of G?teborg,G?teborg,Sweden;4.Department of Virology,University of G?teborg,G?teborg,Sweden
Abstract:

Background  

Cytochalasin B does not directly activate the oxygen-radical-producing NADPH oxidase activity of neutrophils but transfers desensitized G-protein coupled receptors (GPCR) into an active signaling state by uncoupling GCPR from the cytoskeleton. The receptor uncoupling results in respiratory burst activity when signals generated by reactivated formyl peptide receptors trigger the NADPH-oxidase to produce superoxide anions.
Keywords:
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