| Overview |
| bs-4807R-A680 |
| ATXN3L Polyclonal Antibody, ALEXA FLUOR® 680 Conjugated |
| WB, IF(IHC-P), IF(IHC-F), IF(ICC) |
| Human |
| Specifications |
| ALEXA FLUOR® 680 |
| Rabbit |
| KLH conjugated synthetic peptide derived from human ATXN3L |
| 251-355/355 |
| Polyclonal |
| IgG |
| 1ug/ul |
| Purified by Protein A. |
| Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles. |
| Target |
| 92552 |
| Cell membrane |
| ATX3L_HUMAN; ATXN3L; Machado-Joseph disease protein 1-like; MJDL; Putative ataxin-3-like protein. |
| Defects in ATXN3 are the cause of spinocerebellar ataxia type 3 (SCA3) ; also known as Machado-Joseph disease (MJD). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCA3 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. The molecular defect in SCA3 is the a CAG repeat expansion in ATXN3 coding region. Longer expansions result in earlier onset and more severe clinical manifestations of the disease. |
| Application Dilution |
| WB |
1:300-5000 |
| IF(IHC-P) |
1:50-200 |
| IF(IHC-F) |
1:50-200 |
| IF(ICC) |
1:50-200 |
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