Cet anticorps anti-Ataxin 2 Polyclonal Lapin (ABIN7213706) détecte spécifiquement Ataxin 2 dans WB, ELISA, IHC et IF.
L’anticorps est réactif avec des échantillons de Humain et Souris.
Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB 1:500-1:2000,IHC 1:100-1:300,ELISA 1:20000,IF 1:50-200
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
Liquid in PBS containing 50 % glycerol, 0.5 % BSA and 0.02 % 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
-20 °C
Stockage commentaire
Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing.
Date de péremption
12 months
Antigène
Ataxin 2 (ATXN2)
Autre désignation
Ataxin-2
Sujet
ATXN2, ATX2, SCA2, TNRC13, Ataxin-2, Spinocerebellar ataxia type 2 protein, Trinucleotide repeat-containing gene 13 proteinATXN2 belongs to a group of genes that is associated with microsatellite-expansion diseases, a class of neurological and neuromuscular disorders caused by expansion of short stretches of repetitive DNA. The protein (ataxin 2) encoded by ATXN2 has two globular domains near the N-terminus, one of which contains a clathrin-mediated trans-Golgi signal and an endoplasmic reticulum exit signal. The protein is primarily localized to the Golgi apparatus, with deletion of the Golgi and endoplasmic reticulum signals resulting in abnormal subcellular localization. In addition, the N-terminal region contains a polyglutamine tract of 14-31 residues that can be expanded in the pathogenic state to 32-200 residues. Intermediate length expansions of this tract increase susceptibility to amyotrophic lateral sclerosis, while long expansions of this tract result in spinocerebellar ataxia-2, an autosomal-dominantly inherited, neurodegenerative disorder. Alternative splicing results in multiple transcript variants.