Human Azurocidin/CAP37/HBP Antibody
Human Azurocidin/CAP37/HBP Antibody Summary
Accession # P20160
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Azurocidin, also known as cationic antimicrobial protein 37 (CAP37) and heparin-binding protein (HBP), is a member of the serine protease family that includes Cathepsin G, neutrophil elastase (NE), and proteinase 3 (PR3). These proteases are found in the specialized azurophilic granules of neutrophils (1, 2). Human Azurocidin 1 is encoded by the AZU1 gene located in a cluster with NE and PR3 on chromosome 19pter (2). The open reading frame predicts a 251 amino acid (aa) protein with an N-terminal 26 aa signal sequence and a 7 aa propeptide. There are also eight cysteine residues and 3 putative N-linked glycosylation sites (1).
Although Azurocidin 1 shares a significant degree of aa sequence identity with Cathepsin G, NE, and PR3, it lacks serine protease activity due to mutations at two of the three residues in the catalytic triad (His41Ser and Ser175Gly) (1, 3). Crystallographic analysis suggests that the antibacterial activity of Azurocidin is mediated by a hydrophobic pocket (residues 20 to 44) that binds Gram-negative bacteria lipid A. These structural data also imply that the heparin binding capacity is mediated by non-specific electrostatic interactions between the negatively charged heparin molecule and a large patch of positively charged residues near the lipid A binding site (3).
Azurocidin has also been identified as a modulator of endothelial permeability. Neutrophils arriving first at sites of inflammation release Azurocidin, which acts in a paracrine fashion on endothelial cells causing the development of intercellular gaps and allowing leukocyte extravasation. These findings imply that Azurocidin may be a reasonable therapeutic target for a variety of inflammatory disease conditions (4).
- Morgan, J.G. et al. (1991) J. Immunol. 147:3210.
- Zimmer, M. et al. (1992) Proc. Natl. Acad. Sci. USA 89:8215.
- Iverson, L.F. et al. (1997) Nat. Struct. Biol. 4:265.
- Gautam, N. et al. (2001) Nat. Med. 7:1123.
Citations for Human Azurocidin/CAP37/HBP Antibody
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Phenol-soluble modulin ?4 mediates Staphylococcus aureus-associated vascular leakage by stimulating heparin-binding protein release from neutrophils
Sci Rep, 2016;6(0):29373.
Sample Types: Cell Culture Supernates
Applications: ELISA Development
Low anticoagulant heparin targets multiple sites of inflammation, suppresses heparin-induced thrombocytopenia, and inhibits interaction of RAGE with its ligands.
Authors: Rao NV, Argyle B, Xu X, Reynolds PR, Walenga JM, Prechel M, Prestwich GD, MacArthur RB, Walters BB, Hoidal JR, Kennedy TP
Am. J. Physiol., Cell Physiol., 2010;299(1):C97-110.
Sample Types: Recombinant Protein
Applications: ELISA Development
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