IKB alpha / NFKBIA recombinant protein

Recombinant Human IKB alpha / NFKBIA Protein (His tag)

Cat. Num. AAA2545594

• Gene Names: NFKBIA; IKBA; MAD-3; NFKBI
• Purity: > 90 % as determined by SDS-PAGE
• Synonyms: IKB alpha / NFKBIA; Recombinant Human IKB alpha / NFKBIA Protein (His tag); IKBA; MAD-3; NFKBI; IKB alpha / NFKBIA recombinant protein

• Host: E Coli
• Purity/Purification: > 90 % as determined by SDS-PAGE
• Form/Format: Lyophilized from sterile 50mM Tris, 0.5M NaCl, pH 8.0
• Sequence Length: 317

• Application Notes: The recombinant human NFKBIA consisting of 323 amino acids and has a calculated molecular mass of 36.4 kDa. It migrates as an approximately 38 kDa band in SDS-PAGE under reducing conditions.
• Predicted N Terminal: Met
• Preparation and Storage: Samples are stable for up to twelve months from date of receipt at -70 degree C

SDS-PAGE

Related Product Information for IKB alpha / NFKBIA recombinant protein

Background: 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-kappaB 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.

Description: A DNA sequence encoding the human NFKBIA (NP_065390.1) (Phe 2-Leu 317) was expressed, with a polyhistide tag at the N-terminus.

NCBI and Uniprot Product Information

• NCBI GI #: 10092619
• NCBI GeneID: 4792
• NCBI Accession #: NP_065390.1
• NCBI GenBank Nucleotide #: NM_020529.2
• UniProt Accession #: P25963; B2R8L6
• Molecular Weight: 35,609 Da
• NCBI Official Full Name: NF-kappa-B inhibitor alpha
• NCBI Official Synonym Full Names: NFKB inhibitor alpha
• NCBI Official Symbol: NFKBIA
• NCBI Official Synonym Symbols: IKBA; MAD-3; NFKBI
• NCBI Protein Information: NF-kappa-B inhibitor alpha
• UniProt Protein Name: NF-kappa-B inhibitor alpha
• UniProt Gene Name: NFKBIA
• UniProt Synonym Gene Names: IKBA; MAD3; NFKBI; IkB-alpha; IkappaBalpha

NCBI Description

This gene encodes a member of the NF-kappa-B inhibitor family, which contain multiple ankrin repeat domains. The encoded protein interacts with REL dimers to inhibit NF-kappa-B/REL complexes which are involved in inflammatory responses. The encoded protein moves between the cytoplasm and the nucleus via a nuclear localization signal and CRM1-mediated nuclear export. Mutations in this gene have been found in ectodermal dysplasia anhidrotic with T-cell immunodeficiency autosomal dominant disease. [provided by RefSeq, Aug 2011]

Uniprot Description

Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL dimers in the cytoplasm through masking of their nuclear localization signals. On cellular stimulation by immune and proinflammatory responses, becomes phosphorylated promoting ubiquitination and degradation, enabling the dimeric RELA to translocate to the nucleus and activate transcription.