Work with LifeSpan to design a custom immunohistochemistry to address your specific biological question. Outsource the entire localization process without having to
worry about finding and characterizing target specific antibodies, sourcing and validating difficult-to-find tissues, and having the ability to interpret the resulting
immunostaining in relation to complex human pathologies.
TCR Screening Services
Test your therapeutic antibodies in immunohistochemistry against a broad panel of normal frozen human tissue types in order to determine potential unintended binding.
Our non-GLP TCR services are designed on the FDA recommendation outlined in their "Points to Consider in the Manufacture and Testing of Monoclonal Antibody Products for Human Use".
Mouse Monoclonal [clone 4B8] (IgG1,k) to Human CHUK / IKKA / IKK Alpha
Immunofluorescence, Western blot, ELISA
Mouse Monoclonal (IgG1) to Human CHUK / IKKA / IKK Alpha
Human, Monkey, Mouse
Western blot, Immunoprecipitation
Human CHUK / IKKA / IKK Alpha
Human, Monkey, Mouse (tested or 100% immunogen sequence identity)
Western blot (1 µg/ml)
Immunoprecipitation (1 - 2 µg/ml)
Specificity and Use
His-tagged full-length human IKKa/IKK1 protein.
Recognizes human IKK alpha. Species cross-reactivity: mouse and monkey.
Suitable for use in Western Blot and immunoprecipitation. Immunoprecipitation: 1-2 ug/ml. Western Blot: 1 ug/ml. Detects a band at ~85kD. Positive control: Daudi, NIH 3T3, or Raw cells. The applications listed have been tested for the unconjugated form of this product. Other forms have not been tested.
PBS, 0.1% sodium azide. Labeled, Biotin
Short term: +4°C; Long term: Add glycerol (40-50%) -20°C.
Serine kinase that plays an essential role in the NF-kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses. Acts as part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation and phosphorylates inhibitors of NF-kappa-B on serine residues. These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome.