N-terminal peptide of Annexin I (AI/Lipocortin I) that inhibits leukocyte extravasation. Acts as a formyl peptide receptor 1 (FPR1) ligand and stimulates neutrophil NADPH oxidase activation.
(Modifications: Gln-1 = N-terminal amide)
|Storage||Desiccate at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solubility||Soluble to 1 mg/ml in 20% acetonitrile / water|
Preparing Stock Solutions
The following data is based on the product molecular weight 2183.35. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||0.46 mL||2.29 mL||4.58 mL|
|5 mM||0.09 mL||0.46 mL||0.92 mL|
|10 mM||0.05 mL||0.23 mL||0.46 mL|
|50 mM||0.01 mL||0.05 mL||0.09 mL|
References are publications that support the biological activity of the product.
Walther et al (2000) A novel ligand of the formyl peptide receptor: annexin I regulates neutrophil extravasation by interacting with the FPR. Mol.Cell 5 831 PMID: 10882119
Rabiert et al (2007) The N-formyl peptide receptors and the anaphylatoxin C5a receptors: an overview. Biochimie 89 1089 PMID: 17428601
Karlsson et al (2005) 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. J.Leuko.Biol. 78 762
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Keywords: Ac9-25, Ac9-25 supplier, Annexin, I, N-terminal, peptide, Acts, FPR1, ligands, FPRL, Formyl, Peptide, Receptors, 3231, Tocris Bioscience
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