ATXN7 antibody (AA 301-400) (AbBy Fluor® 680)
Quick Overview for ATXN7 antibody (AA 301-400) (AbBy Fluor® 680) (ABIN4996941)
Target
See all ATXN7 AntibodiesReactivity
Host
Clonality
Conjugate
Application
-
-
Binding Specificity
- AA 301-400
-
Cross-Reactivity
- Mouse, Rat
-
Predicted Reactivity
- Human,Dog,Cow,Sheep,Pig,Horse,Rabbit
-
Purification
- Purified by Protein A.
-
Immunogen
- KLH conjugated synthetic peptide derived from human Ataxin 7
-
Isotype
- IgG
-
-
-
-
Application Notes
-
IF(IHC-P) 1:50-200
IF(IHC-F) 1:50-200
IF(ICC) 1:50-200 -
Restrictions
- For Research Use only
-
-
-
Format
- Liquid
-
Concentration
- 1 μg/μL
-
Buffer
- Aqueous buffered solution containing 0.01M TBS ( pH 7.4) with 1 % BSA, 0.03 % Proclin300 and 50 % Glycerol.
-
Preservative
- ProClin
-
Precaution of Use
- This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE, which should be handled by trained staff only.
-
Storage
- -20 °C
-
Storage Comment
- Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles.
-
Expiry Date
- 12 months
-
-
- ATXN7 (Ataxin 7 (ATXN7))
-
Alternative Name
- Ataxin 7
-
Background
-
Synonyms: Ataxin7, Ataxin-7, ADCAII, ATXN 7, OPCA III, OPCA3, SCA 7, SCA7, Spinocerebellar Ataxia 7, Spinocerebellar ataxia type 7 protein, ATX7_HUMAN.
Background: The human ataxin-7 gene, also known as spinocerebellar ataxia 7 or SCA7, maps to chromosome 3p13-p12, has a 2,727-bp open reading frame, and encodes a 892 amino acid protein containing a nuclear localization signal and a polyglutamine tract (1,2). SCA7 is an autosomal dominant neurodegenerative disorder characterized by ataxia and selective neuronal cell loss caused by the expansion of a translated CAG repeat encoding a polyglutamine tract in ataxin-7, which is the SCA7 gene product (3,4). Ataxin-7 is expressed within neurons both affected and unaffected in SCA7 pathology with subcellular localization being variable depending upon the neuronal subtype (5). Polyglutamine expanded in ataxin-7 may carry out its pathogenic effects in the nucleus by altering the matrix-associated nuclear structure and/or by disrupting nucleolar function (6).
Target
-