|Other Names||Ataxin-2, Spinocerebellar ataxia type 2 protein, Trinucleotide repeat-containing gene 13 protein, ATXN2, ATX2, SCA2, TNRC13|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP8898c was selected from the Center region of human ATXN2. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Synonyms||ATX2, SCA2, TNRC13|
|Function||Involved in EGFR trafficking, acting as negative regulator of endocytic EGFR internalization at the plasma membrane.|
|Tissue Location||Expressed in the brain, heart, liver, skeletal muscle, pancreas and placenta. Isoform 1 is predominant in the brain and spinal cord. Isoform 4 is more abundant in the cerebellum. In the brain, broadly expressed in the amygdala, caudate nucleus, corpus callosum, hippocampus, hypothalamus, substantia nigra, subthalamic nucleus and thalamus|
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Provided below are standard protocols that you may find useful for product applications.
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.
Pulst,S.M., et.al., Nat. Genet. 14 (3), 269-276 (1996)Imbert,G., et.al., Nat. Genet. 14 (3), 285-291 (1996)
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