ATXN7 Antikörper (AA 301-400) (AbBy Fluor® 647)
Kurzübersicht für ATXN7 Antikörper (AA 301-400) (AbBy Fluor® 647) (ABIN1390560)
Target
Alle ATXN7 Antikörper anzeigenReaktivität
Wirt
Klonalität
Konjugat
Applikation
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Bindungsspezifität
- AA 301-400
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Kreuzreaktivität
- Maus, Ratte
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Homologie
- Human,Dog,Cow,Sheep,Pig,Horse,Rabbit
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Aufreinigung
- Purified by Protein A.
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Immunogen
- KLH conjugated synthetic peptide derived from human Ataxin 7
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Isotyp
- IgG
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Applikationshinweise
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IF(IHC-P) 1:50-200
IF(IHC-F) 1:50-200
IF(ICC) 1:50-200 -
Beschränkungen
- Nur für Forschungszwecke einsetzbar
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Format
- Liquid
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Konzentration
- 1 μg/μL
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Buffer
- Aqueous buffered solution containing 0.01M TBS ( pH 7.4) with 1 % BSA, 0.03 % Proclin300 and 50 % Glycerol.
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Konservierungsmittel
- ProClin
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Vorsichtsmaßnahmen
- This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE, which should be handled by trained staff only.
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Lagerung
- -20 °C
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Informationen zur Lagerung
- Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles.
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Haltbarkeit
- 12 months
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- ATXN7 (Ataxin 7 (ATXN7))
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Andere Bezeichnung
- Ataxin 7
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Hintergrund
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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
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