SNCAIP anticorps (Internal Region)

N° du produit ABIN350932

Cet anticorps Lapin Polyclonal détecte spécifiquement SNCAIP dans WB et IHC. Il présente une réactivité envers Humain.

Aperçu rapide pour SNCAIP anticorps (Internal Region) (ABIN350932)

Antigène: SNCAIP (Synuclein, alpha Interacting Protein (SNCAIP))

Reactivité: Humain

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp SNCAIP est non-conjugé

Application: Western Blotting (WB), Immunohistochemistry (IHC)

Détail du produit anti-SNCAIP anticorps

Épitope: Internal Region

Fonction: Rabbit antibody to Synphilin-1

Specificité: Specific for Synphilin-1.

Réactivité croisée: Humain

Réactivité croisée (Details): Other species not yet tested.

Purification: IgG

Immunogène: A synthetic peptide from the internal region of human Synphilin-1 (Synphilin 1 alpha synuclein interacting protein) conjugated to an immunogenic carrier protein was used as the antigen.

Isotype: IgG

Information d'application

Indications d'application: IHC WB. A concentration of 10-50,micro,g,ml is recommended. The optimal concentration should be determined by the end user. Not yet tested in other applications.

Restrictions: For Research Use only

Stockage

Format: Lyophilized

Reconstitution: Reconstitute in 500 µl of sterile water. Centrifuge to remove any insoluble material.

Conseil sur la manipulation: Avoid freeze and thaw cycles.

Stock: 4 °C,-20 °C

Stockage commentaire: Maintain the lyophilised/reconstituted antibodies frozen at -20°C for long term storage and refrigerated at 2-8°C for a shorter term. When reconstituting glycerol (1:1) may be added for an additional stability. Avoid freeze and thaw cycles.

Date de péremption: 12 months

Détails sur SNCAIP

Antigène: SNCAIP (Synuclein, alpha Interacting Protein (SNCAIP))

Autre désignation: Synphilin-1

Sujet: Tissue specificity: Widely expressed with highest levels in brain heart and placenta. Defects in SNCAIP are a cause of Parkinson disease (PD). PD is a complex multifactorial disorder that typically manifests after the age of 50 years although early-onset cases (before 50 years) are known. PD generally arises as a sporadic condition but is occasionally inherited as a simple mendelian trait. Although sporadic and familial PD are very similar inherited forms of the disease usually begin at earlier ages and are associated with atypical clinical features. PD is characterized by bradykinesia resting tremor muscular rigidity and postural instability as well as by a clinically significant response to treatment with levodopa. The pathology involves the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies (intraneuronal accumulations of aggregated proteins) in surviving neurons in various areas of the brain. Constructs encoding portions of SNCA and SNCAIP co-transfected in mammalian cells promote cytosolic inclusions resembling the Lewy bodies of Parkinson disease. Coexpression of SNCA SNCAIP and PARK2 result in the formation of Lewy body-like ubiquitin-positive cytosolic inclusions. Familial mutations in PARK2 disrupt the ubiquitination of SNCAIP and the formation of the ubiquitin-positive inclusions. These results provide a molecular basis for the ubiquitination of Lewy body-associated proteins and link PARK2 and SNCA in a common pathogenic mechanism through their interaction with SNCAIP.

UniProt: Q9Y6H5