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Ataxin 1 (ATXN1) (pThr236) Peptide
|Synonyms||ATX1, SCA1, D6S504E, ATXN1, atxn1, Atx1, Sca1, C85907, Ataxin-1, CG4547, dAtx-1, dAtx1, DmelCG4547, sca1|
|1 reference available|
|Price||49.50 $ Plus shipping costs $45.00|
|Availability||Will be delivered in 2 to 3 Business Days|
|Characteristics||Blocking peptide for Phospho-ATXN1-pT236 antibody ABIN389951|
|Specificity||The synthetic peptide sequence used to generate the antibody AP3568a was selected from the region of human Phospho-ATXN1-pT236. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
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. ADCAI is genetically heterogeneous, with five genetic loci, designated spinocerebellar ataxia (SCA) 1, 2, 3, 4 and 6, being assigned to five different chromosomes. ADCAII, which always presents with retinal degeneration (SCA7), and ADCAIII often referred to as the `pure' cerebellar syndrome (SCA5), are most likely homogeneous disorders. Several SCA genes have been cloned and shown to contain CAG repeats in their coding regions. ADCA is caused by the expansion of the CAG repeats, producing an elongated polyglutamine tract in the corresponding protein. The expanded repeats are variable in size and unstable, usually increasing in size when transmitted to successive generations. The function of the ataxins is not known. This locus has been mapped to chromosome 6, and it has been determined that the diseased allele contains 41-81 CAG repeats, compared to 6-39 in the normal allele.
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles|
|Restrictions||For Research Use only|
Lim, Crespo-Barreto, Jafar-Nejad et al.: "Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1." in: Nature, Vol. 452, Issue 7188, pp. 713-8, 2008 (PubMed).