Cerebral cavernous malformations (CCMs) are sporadically acquired or inherited vascular lesions of the central nervous system consisting of clusters of dilated thin-walled blood vessels that predispose individuals to seizures and stroke. Mutations in CCM-1, CCM-2, or CCM-3 lead to cerebral cavernous malformations, one of the most common hereditary vascular diseases of the brain. Endothelial cells within these lesions are the main disease compartments. Here, we show that adenoviral CCM-3 expression inhibits endothelial cell migration, proliferation, and tube formation while down regulation of endogenous CCM-3 results in increased formation of tube- like structures. Adenoviral CCM-3 expression does not induce apoptosis under normal endothelial cell culture conditions but protects endothelial cells from staurosporine-induced cell death. Tyrosine kinase activity profiling suggests that CCM-3 supports PDPK-1/Akt-mediated endothelial cell quiescence and survival. The CCM-1 is fused to a N-terminal His-tag (6x His). It is a 86.5 kDa protein containing 756 amino acid residues.
Human KRIT1 expressed in E.coli
CAT# CSC-CTK0628-20 (20 μg); CAT# CSC-CTK0628-100 (100 μg)
Greater than 90% as determined by SDS-PAGE analysis.
Less than 1 EU/μg.
Lyophilized from a steril-filtered protein solution in urea.
Please centrifuge product briefly before opening vial. The lyophilized protein should be reconstituted in sterile, ultra-pure water to a concentration of 0.1-1.0 mg/ml. This solution can then be diluted into other aqueous buffers and stored at -20°C for future use.
Storage & Stability
The lyophilized protein, though stable at room temperature for up to 3 weeks, is best stored desiccated at -20°C. Reconstituted protein should be used immediately or stored long-term in undiluted working aliquots at -20°C. For long-term storage it is recommended to add a carrier protein (0.1% HSA or BSA). Avoid repeated freeze-thaw cycles.
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