Recombinant Mouse Endostatin Protein, CF

Recombinant Mouse Endostatin Protein, CF Summary

Product Specifications

Product Datasheets

Carrier Free

CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.

In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.

Background: Endostatin

Endostatin, an endogenous non‑glycosylated inhibitor of endothelial cell proliferation and angiogenesis, is an approximately 181 amino acid (aa), 20 kDa proteolytic fragment of the C‑terminal non‑collagenous domain of type XVIII collagen (1, 2). It is produced and/or trimmed by metalloproteinases such as MMP‑2 and MMP‑9, and cathepsins S, B and L (3, 4). The N‑terminal ~27 aa of Endostatin appear to contain the majority of its activity (4, 5). This region contains zinc binding sites that are thought to be critical for its anti‑endothelial and anti‑tumor effects, as well as multiple cleavage sites that, when used, can modify its activity (4, 5). Mouse Endostatin shares 96% aa sequence identity with rat and 85‑87% with human, bovine and equine Endostatin. Endostatin inhibits endothelial cell growth by inducing cell cycle arrest in G1 phase and initiating apoptosis (1, 2). It is also thought to down‑regulate angiogenesis by blocking VEGF‑induced endothelial cell migration (6, 7). It alters the effect of FGF basic on adhesion, proliferation, and cell motility (8). Endostatin can interact with Transglutaminase 2, heparin, and integrins  alpha 5 beta 1 and alpha v beta 3, all of which may be secreted by, or expressed on, endothelial cells, and can influence adhesion or migration (9, 10). Endostatin may also be involved with down‑regulation of angiogenesis after establishment of placental circulation in the pregnant uterus (11). Over-expression in keratinocytes causes delay in healing of excisional wounds, while exogenous systemic Endostatin promotes endothelial and smooth muscle nitric oxide production and decreases blood pressure (12, 13). Since tumor growth and metastasis relies on angiogenesis to provide blood supply, Endostatin is inhibitory for a wide variety of primary and metastatic tumors (5‑8).

Related Research Areas

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