ATXN1 Antibody | 61-519

ATXN1 Antibody | 61-519 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: N/A

Immunogen: This ATXN1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 754-781 amino acids from human ATXN1.

Research Area: Neuroscience

Tested Application: WB, IF

Application: For WB starting dilution is: 1:2000
For IF starting dilution is: 1:10~50

Specificiy: N/A

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 87 kDa

Validation: N/A

Isoform: N/A

Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.

Clonality: Polyclonal

Clone: N/A

Isotype: Rabbit Ig

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.

Concentration: batch dependent

Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Alternate Name: Ataxin-1, Spinocerebellar ataxia type 1 protein, ATXN1, ATX1, SCA1

User Note: Optimal dilutions for each application to be determined by the researcher.

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.