PDCD10
Reaktivität: Human, Maus
WB, IF
Wirt: Kaninchen
Polyclonal
unconjugated
Applikationshinweise
Optimal working dilution should be determined by the investigator.
Beschränkungen
Nur für Forschungszwecke einsetzbar
Rekonstitution
Restore with sterile water to a concentration of 1.0 mg/mL.
Buffer
5 mM PBS, pH 7.2 without preservatives or stabilizers
Konservierungsmittel
Without preservative
Handhabung
Avoid repeated freezing and thawing.
Lagerung
4 °C/-20 °C
Informationen zur Lagerung
The lyophilized antibody can be stored at RT for up to 1 month, or desiccated at -20 °C for longer. Following reconstitution store undiluted at 2-8 °C for one month or (in aliquots) at -20 °C for longer.
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).Synonyms: CCM3, Cerebral cavernous malformations 3 protein, Programmed cell death protein 10, TF-1 cell apoptosis-related protein 15, TFAR15