All IkB alpha reagents are produced in house and quality controlled, including 7 IkB alpha Antibody, 2 IkB alpha ELISA, 32 IkB alpha Gene, 2 IkB alpha IPKit, 1 IkB alpha Protein, 1 IkB alpha qPCR. All IkB alpha reagents are ready to use.
Recombinant IkB alpha proteins are expressed by E. coli with fusion tags as N-His.
IkB alphaantibodies are validated with different applications, which are ELISA(Cap), ELISA, ELISA(Det), FCM, ICC/IF, IF, WB, IP.
IkB alphacDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each IkB alpha of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.
IkB alphaELISA Kit are quality controlled by 8 internation QC standard which guarantee every ELISA Kit with high quality.
Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkB alpha, NFKBIA, or IKBA), is a member of the NF-kappa-B inhibitor family that function to inhibit the NF-kB transcription factor. NFKBIA inhibits NF-kB by masking the nuclear localization signals (NLS) of NF-kB proteins and keeping them sequestered in an inactive state in the cytoplasm. In addition, NFKBIA blocks the ability of NF-κB transcription factors to bind to DNA, which is required for NF-kB's proper functioning. Signal-induced degradation of I kappa B alpha exposes the nuclear localization signal of NF-kappa B, thus allowing it to translocate into the nucleus and activate transcription from responsive genes. An autoregulatory loop is established when NF-kappa B induces expression of the I kappa B alpha gene and newly synthesized I kappa B alpha accumulates in the nucleus where it negatively regulates NF-kappa B-dependent transcription. As part of this post-induction repression, the nuclear export signal on I kappa B alpha mediates transport of NF-kappa B-I kappa B alpha complexes from the nucleus to the cytoplasm. Deletion of NFKBIA has an effect that is similar to the effect of EGFR amplification in the pathogenesis of glioblastoma and is associated with comparatively short survival. Polymorphisms in NFKBIA may be important in pre-disposition to and outcome after treatment, of multiple myeloma (MM). The NFKBIA gene product, IkappaBalpha, binds to NF-kappaB preventing its activation and is important in mediating resistance to apoptosis in B-cell lymphoproliferative diseases.