This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis
Immunogène
This Synphilin-1 (SNCAIP) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 593-622 amino acids from the C-terminal region of human Synphilin-1 (SNCAIP).
SNCAIP
Reactivité: Humain
ELISA
Hôte: Lapin
Polyclonal
HRP
Indications d'application
For WB starting dilution is: 1:1000
Restrictions
For Research Use only
Format
Liquid
Concentration
2 mg/mL
Buffer
Supplied in PBS with 0.09 % (W/V) sodium azide.
Agent conservateur
Sodium azide
Précaution d'utilisation
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
4 °C,-20 °C
Stockage commentaire
Store at 4°C for three months and -20°C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Antigène
SNCAIP
(Synuclein, alpha Interacting Protein (SNCAIP))
Parkinson is the second most common neurodegenerative disease after Alzheimers. About 1 percent of people over the age of 65 and 3 percent of people over the age of 75 are affected by the disease. The mutation is the most common cause of Parkinson disease identified to date. Synuclein alpha interacting protein (Synphilin-1) contains several protein-protein interaction domains and interacts with alpha synuclein in neurons. Mutations of SNCAIP have been linked to Parkinson disease. The amino acid sequence of synphilin-1 shows extensive homology with its human counterpart, especially in regions containing ankyrin-like motifs and the coiled-coil domain. Expression of mouse synphilin-1 in tissues is similar to its human counterpart. Synphilin-1 has an important role in the formation of aggregates and cytotoxicity in Parkinson disease and that Dorfin may be involved in the pathogenic process by ubiquitylation of synphilin-1. Role of synphilin-1 in synaptic function and protein degradation and in the molecular mechanisms leading to neurodegeneration in Parkinson disease