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|Tested species reactivity||Human|
|Published species reactivity||Mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||The epitope recognized by this antibody maps to a C-terminal region between residue 2340 and 2390 of spectrin beta 3.|
|Purification||Antigen affinity chromatography|
|Contains||0.02% sodium azide|
|Storage Conditions||Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.|
|Tested Applications||Dilution *|
|Immunohistochemistry (IHC)||10-20 µg/ml|
|Immunohistochemistry (Paraffin) (IHC (P))||10-20 µg/ml|
|Immunoprecipitation (IP)||2-5 µg/mg lysate|
|Western Blot (WB)||1:2000-1:10,000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Immunohistochemistry (IHC)||See 1 publications below|
Suggested positive control: Hela whole cell extract.
Mutations in spectrins are a previously unknown cause of ataxia and neurodegenerative disease that affect membrane proteins involved in glutamate signaling. Spectrin-beta IIIs have been recognized as ataxia disease genes and their mutations cause spinocerebellar ataxia type 5 (SCA5).
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Prednisolone treatment does not interfere with 2'-O-methyl phosphorothioate antisense-mediated exon skipping in Duchenne muscular dystrophy.
PA1-46007 was used in immunohistochemistry to study the effect of prednisolone treatment on exon skipping in Duchenne muscular dystrophy
|Verhaart IE,Heemskerk H,Karnaoukh TG,Kolfschoten IG,Vroon A,van Ommen GJ,van Deutekom JC,Aartsma-Rus A||Human gene therapy (23:262)||2012|
beta-III spectrin; glutamate transporter EAAT4-associated protein 41; GTRAP41; SCA5; spectrin beta chain, brain 2; spectrin beta III sigma 2; spectrin, beta, non-erythrocytic 2; spectrin, non-erythroid beta chain 2; spinocerebellar ataxia 5 protein
GTRAP41; KIAA0302; SCA5; SCAR14; SPTBN2