The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Peptide ELISA: antibody detection limit dilution: 1/8000.
WB: Use at a concentration of 0.3 - 1 µg/ml. Predicted molecular weight: 13 kDa.
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
Calcium-binding protein. Has antimicrobial activity towards bacteria and fungi. Important for resistance to invasion by pathogenic bacteria. Up-regulates transcription of genes that are under the control of NF-kappa-B. Plays a role in the development of endotoxic shock in response to bacterial lipopolysaccharide (LPS) (By similarity). Promotes tubulin polymerization when unphosphorylated. Promotes phagocyte migration and infiltration of granulocytes at sites of wounding. Plays a role as a pro-inflammatory mediator in acute and chronic inflammation and up-regulates the release of IL8 and cell-surface expression of ICAM1. Extracellular calprotectin binds to target cells and promotes apoptosis. Antimicrobial and proapoptotic activity is inhibited by zinc ions.
Expressed by macrophages in acutely inflammed tissues and in chronic inflammation. Detected in peripheral blood leukocytes, in neutrophils and granulocytes. Detected at sites of vascular inflammation (at protein level). Also expressed in epithelial cells constitutively or induced during dermatoses.
Belongs to the S-100 family. Contains 2 EF-hand domains.
Phosphorylated. Phosphorylation inhibits activation of tubulin polymerization.
Secreted. Cytoplasm. Cytoplasm > cytoskeleton. Cell membrane. Associates with tubulin filaments in activated monocytes. Targeted to the cell surface upon calcium influx. Released from blood leukocytes upon exposure to CSF2/GM-CSF, bacterial lipopolysaccharide (LPS) and during inflammatory processes. Serum levels are high in patients suffering from chronic inflammation.
Tsai SY et al. DAMP molecule S100A9 acts as a molecular pattern to enhance inflammation during influenza A virus infection: role of DDX21-TRIF-TLR4-MyD88 pathway. PLoS Pathog10:e1003848 (2014).
Read more (PubMed: 24391503) »