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Cell Signaling Il-8 (E5f5q) Rabbit mAb (BSA And Azide Free)
List Price
$873.65
Your Price
$873.65
Cell Signaling Il-8 (E5f5q) Rabbit mAb (BSA And Azide Free) - CSIG (Additional S&H or Hazmat Fees May Apply)
NETA PART:
CSIG-10681SF
MFG.PART:
10681SF
UNSPSC:
12352203
Manufacturer:
Cell Signaling
| Size | 100 µg |
| Reactivity | H |
| Sensitivity | Endogenous |
| Molecular Weight (kDa) | 11 |
| Source/Isotype | Rabbit IgG |
| Application/Dilution | {} |
| Storage | Supplied in 1X PBS, BSA and Azide Free. For standard formulation of this product see product #94407. |
| Specificity/Sensitivity | IL-8 (E5F5Q) XP® Rabbit mAb (BSA and Azide Free) recognizes endogenous levels of total IL-8 protein. |
| Species Reactivity | Human |
| Source/Purification | Monoclonal antibody is produced by immunizing animals with human IL-8 recombinant protein. |
| Background | The prototypical CXC chemokine, IL-8, is best known for effects on neutrophils, specifically its ability to act as a chemoattractant and activate degranulation and respiratory burst (1-3).IL-8 is produced by a number of cell types, including monocytes, T cells, neutrophils, fibroblasts, endothelial cells, and others (1). In addition to its effects on neutrophils, IL-8 promotes angiogenesis, inhibits endothelial cell apoptosis, and promotes the proliferation of melanoma cells in an autocrine fashion (1). As a result, IL-8 may be a contributing factor to the development of certain cancers (1,2). There are two distinct receptors for IL-8, CXCR1 and CXCR2; both are g protein-coupled receptors (1). Ligand binding induces Ca2+ mobilization and activates the PI3K, PKC, Rho, and Rac pathways (1,3). |
| SKU | CSIG-10681SF |
|---|---|
| Supplier Part Number | 10681SF |
| UM | EA |
| UNSPSC | 12352203 |
| Manufacturer | Cell Signaling |
| MSDS URL | Click here |
| Temperature | -20C |
| CountryOfOrigin | United States |
| ProductLine | CSIG |
| Qty | 1 |
| MinOrderQty | 1 |
| Weight | 7.000000 |
| Lead Time | 5 |
| Hazardous | N |
| Energy Star | No |
| Green | No |
| Controlled | N |