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PDCD10 Antikörper

Dieses Anti-PDCD10-Antikörper ist ein Kaninchen Polyklonal-Antikörper zur Detektion von PDCD10 in WB und IF. Geeignet für Human.
Produktnummer ABIN1589850

Kurzübersicht für PDCD10 Antikörper (ABIN1589850)

Target

Alle PDCD10 Antikörper anzeigen
PDCD10 (Programmed Cell Death 10 (PDCD10))

Reaktivität

  • 42
  • 28
  • 14
Human

Wirt

  • 55
  • 2
Kaninchen

Klonalität

  • 55
  • 2
Polyklonal

Konjugat

  • 19
  • 5
  • 3
  • 3
  • 2
  • 2
  • 2
  • 2
  • 2
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
Dieser PDCD10 Antikörper ist unkonjugiert

Applikation

  • 22
  • 20
  • 13
  • 13
  • 5
  • 5
  • 3
  • 3
  • 2
  • 2
  • 1
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
  • Applikationshinweise

    Western Blot: Use 1-5 μg/mL

    Beschränkungen

    Nur für Forschungszwecke einsetzbar
  • 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
  • Target

    PDCD10 (Programmed Cell Death 10 (PDCD10))

    Andere Bezeichnung

    CCM-3

    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
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