Key features and details
- Rabbit polyclonal to Senataxin
- Suitable for: ICC/IF
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Senataxin antibody
See all Senataxin primary antibodies
DescriptionRabbit polyclonal to Senataxin
Tested applicationsSuitable for: ICC/IFmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
- A549 cells.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.20
Preservative: 0.02% Sodium azide
Constituents: 40% Glycerol (glycerin, glycerine), 59% PBS
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab220827 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ICC/IF||Use a concentration of 0.25 - 2 µg/ml.
Fixation/Permeabilization: PFA/Triton X-100.
FunctionProbable helicase, which may be involved in RNA maturation (By similarity). Involved in DNA double-strand breaks damage response generated by oxidative stress.
Tissue specificityHighly expressed in skeletal muscle. Expressed in heart, fibroblast, placenta and liver. Weakly expressed in brain and lung. Expressed in the cortex of the kidney (highly expressed in tubular epithelial cells but low expression in the glomerulus).
Involvement in diseaseDefects in SETX are the cause of spinocerebellar ataxia autosomal recessive type 1 (SCAR1) [MIM:606002]; also known as ataxia-ocular apraxia 2. 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. SCAR1 is an autosomal recessive form associated with peripheral neuropathy and elevated serum alpha-fetoprotein, immunoglobulins and, less commonly, creatine kinase levels. Some SCAR1 patients manifest oculomotor apraxia.
Defects in SETX are a cause of amyotrophic lateral sclerosis type 4 (ALS4) [MIM:602433]. ALS4 is a familial form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper and lower motor neurons and resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of cases leading to familial forms. ALS4 is a childhood- or adolescent-onset form characterized by slow disease progression and the sparing of bulbar and respiratory muscles.
Sequence similaritiesBelongs to the DNA2/NAM7 helicase family.
Cellular localizationNucleus > nucleoplasm. Nucleus > nucleolus. Cytoplasm. May be detected in the nucleolus only in cycling cells (By similarity). Most abundant in the nucleus. Detected in granules. Colocalized in cycling cells with FBL in the nucleolus.
- Information by UniProt
- ALS4 antibody
- Amyotrophic lateral sclerosis 4 protein antibody
- AOA2 antibody
ab220827 has been referenced in 3 publications.
- Kannan A et al. ZPR1 prevents R-loop accumulation, upregulates SMN2 expression and rescues spinal muscular atrophy. Brain 143:69-93 (2020). PubMed: 31828288
- Edwards DS et al. BRD4 Prevents R-Loop Formation and Transcription-Replication Conflicts by Ensuring Efficient Transcription Elongation. Cell Rep 32:108166 (2020). PubMed: 32966794
- Kannan A et al. Combined deficiency of Senataxin and DNA-PKcs causes DNA damage accumulation and neurodegeneration in spinal muscular atrophy. Nucleic Acids Res 46:8326-8346 (2018). PubMed: 30010942