PDCD10 antibody (N-Term)

Catalog No. ABIN616008

The Rabbit Polyclonal anti-PDCD10 antibody has been validated for WB and IF. It is suitable to detect PDCD10 in samples from Human.

Quick Overview for PDCD10 antibody (N-Term) (ABIN616008)

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

Binding Specificity: AA 1-212, N-Term

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

Cross-Reactivity (Details): Species reactivity (tested):Human.

Purification: Affinity Chromatography with Immobilized Protein A

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

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Handling

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

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

Preservative: Without preservative

Handling Advice: Avoid repeated freezing and thawing.

Storage: 4 °C/-20 °C

Storage Comment: 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.

Target Details for PDCD10

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

Alternative Name: PDCD10

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).Synonyms: CCM3, Cerebral cavernous malformations 3 protein, Programmed cell death protein 10, TF-1 cell apoptosis-related protein 15, TFAR15

Gene ID: 11235

NCBI Accession: NP_009148

UniProt: Q9BUL8