Product Name: IKAP Antibody
Species Reactivity: Human, Mouse
Tested Applications: ELISA, ICC, IF, WB
Applications: IKAP antibody can be used for detection of IKAP by Western blot at 0.5 to 1 μg/mL. Antibody can also be used for immunocytochemistry starting at 1 μg/mL. For immunofluorescence start at 20 μg/mL.
User Note: Optimal dilutions for each application to be determined by the researcher.
Predicted Molecular Weight: Predicted: 134, 147 kDa Observed: 105, 145 kDa
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.
Host Species: Rabbit
Purification: IKAP Antibody is affinity chromatography purified via peptide column.
Physical State: Liquid
CAS NO.: 502-55-6
Product: Eliglustat (hemitartrate)
Buffer: IKAP Antibody is supplied in PBS containing 0.02% sodium azide.
Concentration: 1 mg/mL
Storage Conditions: 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.
Clonality: Polyclonal
Conjugate: Unconjugated
Alternate Names: IKAP Antibody: FD, DYS, ELP1, IKAP, IKI3, TOT1, Elongator complex protein 1, IkappaB kinase complex-associated protein
Accession NO.: AAC64258
Protein Ino: 3757822
Official Symbol: IKBKAP
Geneid: 8518
Background: IKAP Antibody: IKAP was initially identified as a scaffold protein of the IκB kinase complex that could bind to IKKα, IKKβ, NF-κB, and the NF-κB-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.
PubMed ID:http://aac.asm.org/content/25/5/669.abstract
