PDCD10 anticorps

N° du produit ABIN1589850

Détail du produit anti-PDCD10 anticorps

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

Reactivité: Humain

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp PDCD10 est non-conjugé

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

Fonction: CCM-3 antibody

Specificité: Recombinant human CCM3

Attributs du produit: Chromosomal location: 3q26.1

Purification: Protein A purified

Immunogène: Recombinant human CCM3 (ABIN1589742)

Isotype: IgG

Information d'application

Indications d'application: Western Blot: Use 1-5 μg/mL

Restrictions: For Research Use only

Stockage

Format: Lyophilized

Reconstitution: 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

Conseil sur la manipulation: Centrifuge vial prior to opening. Avoid repeated freeze-thaw cycles.

Stock: 4 °C,-20 °C

Stockage commentaire: 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.

Date de péremption: 24 months

Détails sur PDCD10

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

Autre désignation: CCM-3 (PDCD10 Produits)

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

Sujet: 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).

ID gène: 11235

NCBI Accession: NM_007217, NP_009148

UniProt: Q9BUL8