PDCD10 Rabbit Polyclonal Antibody

CAT#: AP26023PU-L

PDCD10 rabbit polyclonal antibody, Aff - Purified

Product Images

Western Blot using Anti Human CCCM3 antibody. The experiment was performed by Elisabetta Dejana's group. IF OM.IEO-Campus, Milan Italy.

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  Immunofluorescence staining (green) of Human foreskin (cryo-section of unfixed tissue) with anti-Human CCM3 antibody. (K5548, dilution1/50). A) Note specific staining in the epidermis and in the wall of microvessels. B) Negative control of a consecutive section. Nuclei counter-stained with Dapi (blue). <em>Specimen provided by Prof. Dr. J. Wilting, Goettingen.The experiment was performed by the research group of Prof. Dr. J. Wilting, University Göttingen, Germany.</em>

Specifications

Product Data

• Applications: IF, WB
• Recommended Dilution: Western Blot: 1-5 μg/ml.
  Immunofluorescence: 2-10 µg/ml.
  Immunohistochemistry.
• Reactivities: Human
• Host: Rabbit
• Clonality: Polyclonal
• Immunogen: Highly pure (> 95%) recombinant Human CCM3, amino acids Met1-Ala212 derived from E.coli (Cat.-No AR26004PU-N)
• Specificity: This antibody will detect recombinant Human CCM-3 in Western Blot and native CCM-3 in Immunohistochemistry.
• Formulation: 5mM PBS, pH 7.2 without preservatives or stabilizers
  State: Aff - Purified
  State: Lyophilized purified IgG fraction
• Reconstitution Method: Restore with sterile water to a concentration of 1.0 mg/ml.
• Purification: Affinity Chromatography with Immobilized Protein A
• Conjugation: Unconjugated
• Storage: Store lyophilized at 2-8°C for 6 months or at -20°C long term.
  After reconstitution store the antibody undiluted at 2-8°C for one month
  or (in aliquots) at -20°C long term.
  Avoid repeated freezing and thawing.
• Stability: Shelf life: one year from despatch.
• Gene Name: programmed cell death 10
• Database Link:
  Entrez Gene 11235 Human
  UniProt ID Q9BUL8
• Background: 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).
• Synonyms: CCM3, TFAR15

Reference Data

• Protein Families: Druggable Genome