详细说明
Purity
>95%, by SDS-PAGE under reducing conditions and visualized by silver stain
Endotoxin Level
<0.10 EU per 1 μg of the protein by the LAL method.
Activity
Measured by the ability of the immobilized protein to support the adhesion of BCE C/D‑1b bovine corneal endothelial cells.
When 4 x 104 cells per well are added to rhBAI1 coated plates (0.5 μg/mL, 100 μL/well), approximately 40%-70% will adhere after 1 hour at 37° C.
Optimal dilutions should be determined by each laboratory for each application.
Source
Chinese Hamster Ovary cell line, CHO-derived Ala31-Thr879, with a C-terminal 6-His tag
Accession #
N-terminal Sequence
AnalysisAla31
Predicted Molecular Mass
93.6 kDa
SDS-PAGE
105-115 kDa, reducing conditions
4969-BA |
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Formulation Lyophilized from a 0.2 μm filtered solution in PBS. | ||
Reconstitution Reconstitute at 200 μg/mL in PBS. | ||
Shipping The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. | ||
Stability & Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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Background: BAI1
Brain Angiogenesis Inhibitor 1 (BAI1) is a 170 kDa 7-transmembrane domain G protein-coupled receptor (GPCR) that has a large N-terminal extracellular region with an RGD motif, five thrombospondin type I repeats, and a juxtamembrane GPS (GPCR proteolytic cleavage site) (1). Within the extracellular domain (ECD) up to the GPS (amino acids 31 - 879), mature human BAI1 shares 94% amino acid sequence identity with mouse and rat BAI1. BAI1 is preferentially expressed on brain neurons but also is found on astrocytes and macrophages and in the pancreas, stomach, and colon (1 - 8). BAI1 can be cleaved within the GPS to release a 120 kDa fragment termed Vasculostatin which corresponds to nearly the entire N-terminal ECD (9). Generation of additional soluble fragments suggests the cleavage of BAI1 at multiple sites (9, 10). BAI1 fragments interact with Integrin alpha V beta 5 or CD36 on microvascular endothelial cells to inhibit cell proliferation and migration (10, 11). Overexpression of BAI1 in glioblastoma or pancreatic adenocarcinoma cells inhibits their tumorigenicity and the development of tumor-associated neovascularization (6, 12). Fragments of the ECD, including Vasculostatin, also suppress in vivo angiogenesis and tumor growth (1, 9, 11). BAI1 is downregulated in glioblastoma, carcinomas of the pancreas, colon, and stomach and also in experimental ischemia (2, 4, 6 - 8). Its expression is inversely correlated with tumor vascularity in colorectal and pulmonary carcinomas (8, 13). On macrophages and astrocytes, BAI1 mediates the phagocytosis of apoptotic cells through recognition of cell surface phosphatidylserine (5).
References:
Nishimori, H. et al. (1997) Oncogene 15:2145.
Koh, J.T. et al. (2001) Brain Res. Mol. Brain Res. 87:223.
Mori, K. et al. (2002) Neurosci. Res. 43:69.
Kaur, B. et al. (2003) Am. J. Pathol. 162:19.
Park, D. et al. (2007) Nature 450:430.
Duda, D.G. et al. (2002) Br. J. Cancer 86:490.
Lee, J.H. et al. (2001) Int. J. Oncol. 18:355.
Fukushima, Y. et al. (1998) Int. J. Oncol. 13:967.
Kaur, B. et al. (2005) Oncogene 24:3632.
Koh, J.T. et al. (2004) Exp. Cell Res. 294:172.
Kaur, B. et al. (2009) Cancer Res. 69:1212.
Kang, X. et al. (2006) Cancer Gene Ther. 13:385.
Hatanaka, H. et al. (2000) Int. J. Mol. Med. 5:181.
Long Name:
Brain-specific Angiogenesis Inhibitor 1
Entrez Gene IDs:
575 (Human); 107831 (Mouse); 362931 (Rat)
Alternate Names:
BAI1; brain-specific angiogenesis inhibitor 1; FLJ41988; GDAIF