PDCD10 antibody

Catalog No. ABIN1589850

The Rabbit Polyclonal anti-PDCD10 antibody (ABIN1589850) specifically detects PDCD10 in WB and IF. The antibody is reactive with Human samples.

Quick Overview for PDCD10 antibody (ABIN1589850)

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

Reactivity: Human

Host: Rabbit

Clonality: Polyclonal

Conjugate: This PDCD10 antibody is un-conjugated

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

Product Details anti-PDCD10 Antibody

Purpose: Rabbit Anti-Human CCM-3 Polyclonal Antibody

Specificity: Recombinant human CCM3

Characteristics: Chromosomal location: 3q26.1

Purification: Protein A purified

Immunogen: Recombinant human CCM3 (ABIN1589742)

Isotype: IgG

Application Details

Application Notes: Western Blot: Use 1-5 μg/mL

Restrictions: For Research Use only

Handling

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 Details for PDCD10

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

Alternative Name: CCM-3

Background:

Synonyms: PDCD10, CCM3, TFAR15, programmed cell death 10

Description: 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