Der Kaninchen Polyklonal Anti-IKAP/p150-Antikörper wurde für WB, ELISA, ICC und IF validiert. Er ist geeignet, IKAP/p150 in Proben von Human und Maus zu detektieren.
Produktnummer ABIN6990353
Kurzübersicht für IKAP/p150 Antikörper (C-Term) (ABIN6990353)
At least two isoforms of IKAP are known two exist, this antibody will detect both isoforms.
Aufreinigung
IKAP Antibody is affinity chromatography purified via peptide column.
Immunogen
IKAP antibody was raised against a 16 amino acid synthetic peptide from near the carboxy terminus of human IKAP. The immunogen is located within the last 50 amino acids of IKAP.
IKAP antibody can be used for detection of IKAP by Western blot at 0.5 to 1 μ,g/mL. Antibody can also be used for immunocytochemistry starting at 1 μ,g/mL. For immunofluorescence start at 20 μ,g/mL.
Antibody validated: Western Blot in mouse samples, Immunocytochemistry in mouse samples and Immunofluorescence in mouse samples. All other applications and species not yet tested.
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Konzentration
1 mg/mL
Buffer
IKAP Antibody is supplied in PBS containing 0.02 % sodium azide.
Konservierungsmittel
Sodium azide
Vorsichtsmaßnahmen
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Lagerung
-20 °C,4 °C
Informationen zur Lagerung
IKAP antibody can be stored at 4°C for three months and -20°C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Target
IKAP/p150 (ELP1)
(Elongator Complex Protein 1 (ELP1))
Andere Bezeichnung
IKAP
Hintergrund
IKAP Antibody: IKAP was initially identified as a scaffold protein of the Iκ,B kinase complex that could bind to IKKα, IKKβ, NF-κ,B, and the NF-κ,B-inducing kinase (NIK), although later evidence has cast doubt on this. More recent reports show that mutations in IKAP such as a frameshift leading to a truncated protein or a missense mutation that leads to defective phosphorylation are responsible for the autosomal recessive genetic disease familial dysautonomia (FD). Reports indicating that it forms part of the RNA polymerase II transcription elongation complex suggest that this disease may be due to compromised transcription elongation. More recently, it was shown that IKAP associates with c-Jun N-terminal kinase (JNK) and could specifically enhance JNK activation induced by the upstream JNK activators MEKK1 and ASK1, indicating another possible cause for FD.