Till sidans topp

Sidansvarig: Webbredaktion
Sidan uppdaterades: 2012-09-11 15:12

Tipsa en vän
Utskriftsversion

Neutrophil NADPH-oxidase … - Göteborgs universitet Till startsida
Webbkarta
Till innehåll Läs mer om hur kakor används på gu.se

Neutrophil NADPH-oxidase activation by an annexin AI peptide is transduced by the formyl peptide receptor (FPR), whereas an inhibitory signal is generated independently of the FPR family receptors

Artikel i vetenskaplig tidskrift
Författare Jennie Karlsson
Huamei Fu
F. Boulay
Claes Dahlgren
Kristoffer Hellstrand
Charlotta Movitz
Publicerad i Journal of leukocyte biology
Volym 78
Nummer/häfte 3
Sidor 762-71
ISSN 0741-5400 (Print)
Publiceringsår 2005
Publicerad vid Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning
Institutionen för laboratoriemedicin, Avdelningen för klinisk virologi
Sidor 762-71
Språk en
Länkar dx.doi.org/10.1189/jlb.0305153
Ämnesord Annexin A1/immunology, Calcium/metabolism, Cell Differentiation/drug effects, Enzyme Activation/drug effects, HL-60 Cells, Humans, N-Formylmethionine Leucyl-Phenylalanine/pharmacology, NADPH Oxidase/antagonists & inhibitors/*immunology, Neutrophils/drug effects/*enzymology/immunology, Receptors, Formyl Peptide/*antagonists & inhibitors/immunology, Signal Transduction/*drug effects/immunology, Superoxides/antagonists & inhibitors/metabolism, Time Factors
Ämneskategorier Mikrobiologi inom det medicinska området

Sammanfattning

Truncation of the N-terminal part of the calcium-regulated and phospholipid-binding protein annexin AI has been shown to change the functional properties of the protein and to generate immunoregulatory peptides. Proinflammatory as well as anti-inflammatory signals are triggered by these peptides, and the two formyl peptide receptor (FPR) family members expressed in neutrophils, FPR and FPR-like 1 (FPRL1), have been suggested to transduce these signals. We now report that an annexin AI peptide (Ac9-25) activates, as well as inhibits, the neutrophil release of superoxide anions. Results obtained from experiments with receptor antagonists/inhibitors, desensitized cells, and transfected cells reveal that the Ac9-25 peptide activates the neutrophil reduced nicotinamide adenine dinucleotide phosphate oxidase through FPR but not through FPRL1. The Ac9-25 peptide also inhibits the oxidase activity in neutrophils triggered, not only by the FPR-specific agonist N-formyl-Met-Leu-Phe but also by several other agonists operating through different G protein-coupled receptors. Our data show that the two signals generated by the Ac9-25 peptide are transmitted through different receptors, the inhibitory signal being transduced by a not-yet identified receptor distinct from FPR and FPRL1.

Sidansvarig: Webbredaktion|Sidan uppdaterades: 2012-09-11
Dela:

På Göteborgs universitet använder vi kakor (cookies) för att webbplatsen ska fungera på ett bra sätt för dig. Genom att surfa vidare godkänner du att vi använder kakor.  Vad är kakor?