PDCD10 anticorps (N-Term)

N° du produit ABIN616008

L’anticorps Lapin Polyclonal anti-PDCD10 a été validé pour WB et IF. Il convient pour détecter PDCD10 dans des échantillons de Humain.

Aperçu rapide pour PDCD10 anticorps (N-Term) (ABIN616008)

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)

Détail du produit anti-PDCD10 anticorps

Épitope: AA 1-212, N-Term

Specificité: This antibody will detect recombinant Human CCM-3 in Western Blot and native CCM-3 in Immunohistochemistry.

Réactivité croisée (Details): Species reactivity (tested):Human.

Purification: Affinity Chromatography with Immobilized Protein A

Immunogène: Highly pure (> 95%) recombinant Human CCM3, amino acids Met1-Ala212 derived from E.coli

Information d'application

Indications d'application: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Stockage

Reconstitution: Restore with sterile water to a concentration of 1.0 mg/mL.

Buffer: 5 mM PBS, pH 7.2 without preservatives or stabilizers

Agent conservateur: Without preservative

Conseil sur la manipulation: Avoid repeated freezing and thawing.

Stock: 4 °C/-20 °C

Stockage commentaire: 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.

Détails sur PDCD10

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

Autre désignation: PDCD10

Sujet: 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

ID gène: 11235

NCBI Accession: NP_009148

UniProt: Q9BUL8