Recombinant Mouse Brevican Protein, CF Summary
When Recombinant Mouse Brevican is coated at 3 μg/mL (100 μL/well), the concentration of biotinylated hyaluronan that produces 50% of the optimal binding response is found to be approximately 1-6 ng/mL.
Met1-Leu883, with a C-terminal 6-His tag
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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.
|Formulation||Lyophilized from a 0.2 μm filtered solution in PBS.|
|Reconstitution||Reconstitute at 100 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.
Brevican, also called BEHAB, is a member of the the lectican family of proteoglycans that share a common domain structure (1). It is restricted to the CNS and associates with perineuronal nets and astrocytes (2 ‑ 5). Brevican contains an Ig-like V-set domain, two link domains, a Glu-rich region, a central region with glycosaminoglycan (GAG) modifications, an EGF-like domain, a C-type lectin domain, and a C-terminal Sushi/CRP-like domain (6). Brevican consists of a 145 kDa core protein with up to approximately 100 kDa of attached chondroitin sulfate but not heparan sulfate chains (3, 7). Alternate splicing generates a GPI-anchored isoform that lacks the EGF-like, lectin, and Sushi domains (4, 6). Brevican is cleaved by multiple proteases and exists in a number of distinct fragments (8, 9). An under-glycosylated form of Brevican accumulates in highly aggressive glioma, Alzheimer’s-like brain, and following brain injury (10 - 12). Levels of an ADAMTS-generated 55 kDa N-terminal fragment accumulate during remodeling after excitotoxic injury, and Brevican cleavage is required for its ability to promote glioma adhesion and motility (13 ‑ 15). In contrast, Brevican cleavage is inhibited in mouse brain with amyloid beta deposits (10). Mouse Brevican shares 80%, 81%, and 95% aa sequence identity with bovine, human, and rat Brevican, respectively. Within the Ig-like and two link domains, mouse Brevican shares 47% - 51% aa sequence identity with mouse Aggrecan, Neurocan, and Versican.
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