Background:   The NF-kappa-B (NFKB) complex of proteins is inhibited by I-kappa-B (IKB) proteins, which inactivate NFKB by trapping it in the cytoplasm. Phosphorylation of serine residues on the IKB proteins by IKB kinases marks them for destruction via the ubiquitination pathway, thereby allowing activation and nuclear translocation of the NFKB complex. The protein encoded by this gene is similar to IKB kinases and can mediate NFKB activation in response to certain growth factors. Serine/threonine protein involved in the signaling cascade converging to the activation of the transcription factor NF-kappa-B. May function as an IKK kinase, playing an essential role in the transcription of a subset of TNF-alpha-induced genes. Also mediates production of RANTES/CCL5 and interferon-beta/IFNB1. Has a pivotal role in the innate immune response. Phosphorylates Borna disease virus (BDV) P protein. Phosphorylates and activates IRF3 and IRF7 and allows their nuclear localization. This leads to production of alpha/beta interferons and the development of a cellular antiviral state. It also seems to be a central factor in the induction of the antiviral interferon response. Inhibition of its interaction with IRF3, due to HCV NS3 binding or BDV P protein seems to be one mechanism of inhibition of the innate immune responses of hepatitis C virus (HCV) infection or Borna disease virus infection respectively.

Description: Rabbit polyclonal to TBK1

Immunogen: KLH conjugated synthetic peptide derived from TBK1

Specificity:  ·Reacts with Human, Mouse and Rat.

.·Isotype: IgG

Application:  ·Western blotting: 1/100-500. Predicted Mol wt: 84 kDa;

·Immunohistochemistry (Paraffin/frozen tissue section): 1/50-200;

·Immunocytochemistry/Immunofluorescence: 1/100;

·Immunoprecipitation: 1/50;

·ELISA: 1/500;

·Optimal working dilutions must be determined by the end user.