Application Note
*Optimal dilutions/concentrations should be determined by the researcher.
Application |
Recommended Dilution |
1:500-1:3000 |
1:100-1:1000 |
Assay dependent |
Not tested in other applications.
Calculated MW
Positive Control
293T , A431 , HeLa , HepG2
Form
Liquid
Buffer
PBS, 1% BSA, 20% Glycerol
Preservative
0.025% ProClin 300
Storage
Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.
Concentration
0.2 mg/ml (Please refer to the vial label for the specific concentration.)
Antigen Species
Human
Immunogen
Recombinant protein encompassing a sequence within the center region of human ATXN2. The exact sequence is proprietary.
Purification
Purified by antigen-affinity chromatography.
Conjugation
Unconjugated
RRID
AB_2885139
Note
For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.
Synonyms
ataxin 2 , ATX2 , SCA2 , TNRC13
Cellular Localization
Cytoplasm
Background
The autosomal dominant cerebellar ataxias (ADCA) are a heterogeneous group of neurodegenerative disorders characterized by progressive degeneration of the cerebellum, brain stem and spinal cord. Clinically, ADCA has been divided into three groups: ADCA types I-III. Defects in this gene are the cause of spinocerebellar ataxia type 2 (SCA2). SCA2 belongs to the autosomal dominant cerebellar ataxias type I (ADCA I) which are characterized by cerebellar ataxia in combination with additional clinical features like optic atrophy, ophthalmoplegia, bulbar and extrapyramidal signs, peripheral neuropathy and dementia. SCA2 is caused by expansion of a CAG repeat in the coding region of this gene. Longer expansions result in earlier onset of the disease. Alternatively spliced transcript variants encoding different isoforms have been identified but their full length sequence has not been determined. [provided by RefSeq]
Database
Research Area