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ATXN7 antibody

The Rabbit Polyclonal anti-ATXN7 antibody has been validated for ELISA and IHC. It is suitable to detect ATXN7 in samples from Human and Mouse.
Catalog No. ABIN7254688

Quick Overview for ATXN7 antibody (ABIN7254688)

Target

See all ATXN7 Antibodies
ATXN7 (Ataxin 7 (ATXN7))

Reactivity

  • 31
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  • 20
  • 3
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  • 3
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  • 2
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  • 1
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Human, Mouse

Host

  • 46
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Rabbit

Clonality

  • 46
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Polyclonal

Conjugate

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  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
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  • 1
This ATXN7 antibody is un-conjugated

Application

  • 36
  • 19
  • 13
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ELISA, Immunohistochemistry (IHC)
  • Characteristics

    Polyclonal Antibody

    Purification

    Antigen affinity purification

    Immunogen

    Synthetic peptide of human ATXN7

    Isotype

    IgG
  • Application Notes

    IHC 1:50-1:300, ELISA 1:5000-1:10000

    Restrictions

    For Research Use only
  • Format

    Liquid

    Concentration

    0.9 mg/mL

    Buffer

    PBS with 0.05 % Sodium azide and 40 % Glycerol, pH 7.4

    Preservative

    Sodium azide

    Precaution of Use

    This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

    Storage

    -20 °C

    Storage Comment

    Store at -20°C. Avoid freeze / thaw cycles.
  • Target

    ATXN7 (Ataxin 7 (ATXN7))

    Alternative Name

    ATXN7

    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. This locus has been mapped to chromosome 3, and it has been determined that the diseased allele associated with spinocerebellar ataxia-7 contains 38-130 CAG repeats (near the N-terminus), compared to 7-17 in the normal allele. The encoded protein is a component of the SPT3/TAF9/GCN5 acetyltransferase (STAGA) and TBP-free TAF-containing (TFTC) chromatin remodeling complexes, and it thus plays a role in transcriptional regulation. Alternative splicing results in multiple transcript variants.

    UniProt

    O15265
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