PDCD10 Antikörper

Produktnummer ABIN1589850

Produktdetails anti-PDCD10 Antikörper

Target: PDCD10 (Programmed Cell Death 10 (PDCD10))

Reaktivität: Human

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Dieser PDCD10 Antikörper ist unkonjugiert

Applikation: Western Blotting (WB), Immunofluorescence (IF)

Verwendungszweck: CCM-3 antibody

Spezifität: Recombinant human CCM3

Produktmerkmale: Chromosomal location: 3q26.1

Aufreinigung: Protein A purified

Immunogen: Recombinant human CCM3 (ABIN1589742)

Isotyp: IgG

Anwendungsinformationen

Applikationshinweise: Western Blot: Use 1-5 μg/mL

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Lyophilized

Rekonstitution: Centrifuge vial prior to opening. Reconstitute in sterile water to a concentration of 0.1-1.0 mg/mL.

Buffer: 0.5X PBS, pH 7.2

Handhabung: Centrifuge vial prior to opening. Avoid repeated freeze-thaw cycles.

Lagerung: 4 °C,-20 °C

Informationen zur Lagerung: The lyophilized antibody is stable for at least 2 years at -20°C. After sterile reconstitution the antibody is stable at 2-8°C for up to 6 months. Frozen aliquots are stable for at least 6 months when stored at -20°C. Addition of a carrier protein or 50% glycerol is recommended for frozen aliquots.

Haltbarkeit: 24 months

Details zu PDCD10

Target: PDCD10 (Programmed Cell Death 10 (PDCD10))

Andere Bezeichnung: CCM-3 (PDCD10 Produkte)

Synonyme: CCM3 antikoerper, TFAR15 antikoerper, 2410003B13Rik antikoerper, Ccm3 antikoerper, Tfa15 antikoerper, Tfar15 antikoerper, zgc:85629 antikoerper, ccm3a antikoerper, pdcd10 antikoerper, zgc:65826 antikoerper, programmed cell death 10 antikoerper, programmed cell death 10 S homeolog antikoerper, programmed cell death 10b antikoerper, programmed cell death 10a antikoerper, PDCD10 antikoerper, Pdcd10 antikoerper, pdcd10.S antikoerper, pdcd10b antikoerper, pdcd10a antikoerper

Hintergrund: PDCD10, CCM3, TFAR15, programmed cell death 10,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).

Gen-ID: 11235

NCBI Accession: NM_007217, NP_009148

UniProt: Q9BUL8