SCN9A Antikörper (AA 1751-1946) (Biotin)
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- Target Alle SCN9A Antikörper anzeigen
- SCN9A (Sodium Channel, Voltage-Gated, Type IX, alpha Subunit (SCN9A))
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Bindungsspezifität
- AA 1751-1946
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Reaktivität
- Human
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Wirt
- Maus
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Klonalität
- Monoklonal
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Konjugat
- Dieser SCN9A Antikörper ist konjugiert mit Biotin
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Applikation
- Immunohistochemistry (IHC), Western Blotting (WB), Immunofluorescence (IF), Immunoprecipitation (IP), Immunocytochemistry (ICC), Antibody Array (AA)
- Spezifität
- Detects ~230 kDa. No cross-reactivity against other Nav channels.
- Kreuzreaktivität
- Hamster, Human, Maus, Ratte
- Aufreinigung
- Protein G Purified
- Immunogen
- Fusion protein amino acids 1751-1946 (C-terminus) of human Nav1.7
- Klon
- N68-6 (Formerly S68-6)
- Isotyp
- IgG1
- Top Product
- Discover our top product SCN9A Primärantikörper
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- Applikationshinweise
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- WB (1:1000)
- IHC (1:1000)
- ICC/IF (1:100)
- optimal dilutions for assays should be determined by the user.
- Kommentare
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1 μg/ml of ABIN2483097 was sufficient for detection of Nav1.7 in 10 μg of HEK-293 cell lysate transiently expressing Nav1.7 by colorimetric immunoblot analysis using Goat anti-mouse IgG:HRP as the secondary antibody.
- Beschränkungen
- Nur für Forschungszwecke einsetzbar
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- Format
- Liquid
- Konzentration
- 1 mg/mL
- Buffer
- PBS pH 7.4, 50 % glycerol, 0.09 % sodium azide, Storage buffer may change when conjugated
- Konservierungsmittel
- Sodium azide
- Vorsichtsmaßnahmen
- This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
- Lagerung
- 4 °C
- Informationen zur Lagerung
- Conjugated antibodies should be stored at 4°C
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- Target
- SCN9A (Sodium Channel, Voltage-Gated, Type IX, alpha Subunit (SCN9A))
- Andere Bezeichnung
- Nav1.7 (SCN9A Produkte)
- Hintergrund
- Nav1.7 is a voltage-gated sodium channel and plays a critical role in the generation and conduction of action potentials and is thus important for electrical signaling by most excitable cells. Therapeutically, the association of pain insensitivity with the loss of function of a certain sodium channel may have implications. Since Nav1.7 is not present in cardiac muscle or neurons in the central nervous system, blockers of Nav1.7 will not have direct action on these cells and thus can have less side effects than current pain medications. By performing more studies, there is a possibility to develop a new generation of drugs that can reduce the pain intensity in animals (1-3).
- Gen-ID
- 6335
- NCBI Accession
- NP_002968
- UniProt
- Q15858
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