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PDCD10 antibody

This anti-PDCD10 antibody is a Rabbit Polyclonal antibody detecting PDCD10 in WB and IF. Suitable for Human.
Catalog No. ABIN1589850

Quick Overview for PDCD10 antibody (ABIN1589850)

Target

See all PDCD10 Antibodies
PDCD10 (Programmed Cell Death 10 (PDCD10))

Reactivity

  • 40
  • 27
  • 13
Human

Host

  • 53
  • 2
Rabbit

Clonality

  • 53
  • 2
Polyclonal

Conjugate

  • 17
  • 5
  • 3
  • 3
  • 2
  • 2
  • 2
  • 2
  • 2
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
This PDCD10 antibody is un-conjugated

Application

  • 20
  • 19
  • 13
  • 13
  • 5
  • 5
  • 3
  • 3
  • 2
  • 2
  • 1
Western Blotting (WB), Immunofluorescence (IF)
  • Purpose

    CCM-3 antibody

    Specificity

    Recombinant human CCM3

    Characteristics

    Chromosomal location: 3q26.1

    Purification

    Protein A purified

    Immunogen

    Recombinant human CCM3 (ABIN1589742)

    Isotype

    IgG
  • Application Notes

    Western Blot: Use 1-5 μg/mL

    Restrictions

    For Research Use only
  • 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

    Handling Advice

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

    Storage

    4 °C,-20 °C

    Storage Comment

    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.

    Expiry Date

    24 months
  • Target

    PDCD10 (Programmed Cell Death 10 (PDCD10))

    Alternative Name

    CCM-3

    Background

    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).

    Gene ID

    11235

    NCBI Accession

    NM_007217, NP_009148

    UniProt

    Q9BUL8
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