Human CCM-3, His-Tag recombinant Protein
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PDCD10, CCM3, TFAR15, programmed cell death 10
Description of Human CCM-3, His-Tag
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 CCM1, CCM2, or CCM3 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 CCM3 expression inhibits endothelial cell migration, proliferation, and tube formation while down regulation of endogenous CCM3 results in increased formation of tube-like structures. Adenoviral CCM3 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 CCM3 supports PDPK-1/Akt-mediated endothelial cell quiescence and survival (Schleider et al, Neurogenetics 12, 2011). The CCM-3 is fused to a N-terminal His-tag (6x His).
Testing in Progress.
The lyophilized CCM3 is soluble in water and most aqueous buffers and should be reconstituted in water or PBS.
Amino Acid Sequence
MGSSHHHHHH SSGLVPRGSM RMTMEEMKNE AETTSMVSMP LYAVMYPVFN ELERVNLSAA QTLRAAFIKA EKENPGLTQD IIMKILEKKS VEVNFTESLL RMAADDVEEY MIERPEPEFQ DLNEKARALK QILSKIPDEI NDRVRFLQTI KDIASAIKEL LDTVNNVFKK YQYQNRRALE HQKKEFVKYS KSFSDTLKTY FKDGKAINVF VSANRLIHQT NLILQTFKTV A
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