NFKBIA anticorps (Ser32, Ser36)

N° du produit ABIN197304

Détail du produit anti-NFKBIA anticorps

Antigène: NFKBIA (Nuclear Factor of kappa Light Polypeptide Gene Enhancer in B-Cells Inhibitor, alpha (NFKBIA))

Épitope: Ser32, Ser36

Reactivité: Humain, Souris

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp NFKBIA est non-conjugé

Application: Western Blotting (WB), Immunofluorescence (IF), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))

Specificité: IkappaB-alpha antibody detects endogenous levels of total IkappaB-alpha protein.

Purification: Immunoaffinity chromatography

Immunogène: Synthetic non-phosphopeptide derived from human IkappaB-alpha around the phosphorylation site of serine 32/36 (H-D-Sp-G-L-D-Sp-M-K).

Information d'application

Indications d'application: Suitable for use in Western blot (1: 500-1: 1000) and Immunohistochemistry (1: 50-1: 100).
Other applications not tested.
Optimal dilutions are dependent on conditions and should be determined by the user.

Restrictions: For Research Use only

Stockage

Concentration: 1.0 mg/mL

Buffer: PBS (without Mg2+ and Ca2+), pH 7.4, 150 mM NaCl, 0.02 % Sodium Azide and 50 % Glycerol.

Agent conservateur: Sodium azide

Précaution d'utilisation: This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Conseil sur la manipulation: Avoid repeated freezing and thawing.

Stock: -20 °C

Stockage commentaire: Store the antibody (in aliquots) at -20 °C.

Références pour anticorps anti-NFKBIA (ABIN197304)

Tsolou, Liousia, Kalamida, Pouliliou, Giatromanolaki, Koukourakis: "Inhibition of IKK-NFκB pathway sensitizes lung cancer cell lines to radiation." dans: Cancer biology & medicine, Vol. 14, Issue 3, pp. 293-301, (2017) (PubMed).

Détails sur NFKBIA

Antigène: NFKBIA (Nuclear Factor of kappa Light Polypeptide Gene Enhancer in B-Cells Inhibitor, alpha (NFKBIA))

Autre désignation: NFKBIA / IKBA (NFKBIA Produits)

Synonymes: anticorps IKBA, anticorps MAD-3, anticorps NFKBI, anticorps AI462015, anticorps Nfkbi, anticorps RL/IF-1, anticorps ECI-6/IKBA, anticorps NFKBIA, anticorps ikbaB, anticorps wu:fb81f08, anticorps zgc:56666, anticorps zgc:77616, anticorps ikbaA, anticorps wu:fj16a07, anticorps zgc:85769, anticorps NFKB inhibitor alpha, anticorps nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha, anticorps nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha b, anticorps nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha a, anticorps NFKBIA, anticorps Nfkbia, anticorps nfkbiab, anticorps nfkbiaa

Sujet: Three major forms of IKB like molecules have been identified and each is characterised by multiple copies of ankyrin repeats. IkappaB alpha and IkappaB beta appear to be the major regulatory forms of IKB in most cells. These proteins interact with p65 or cRel containing forms of NFkappaB and block nuclear import by masking the nuclear localisation sequences of NFkappaB. The activation of NFkappaB involves the inducible phosphorylation and subsequent degradation of IkappaB. Immunoblotting easily detects the hyperphosphorylated forms of IkappaB alpha, but not phosphorylated IkappaB beta. Interestingly, IkappaB alpha and IkappaB beta mediate different NFkappaB responses. IkappaB alpha appears to control more transient activation of NFkappaB in response to an inducer, while IkappaB beta controls a persistent response. Bcl3 interacts with p50 and p52 containing forms of NFkappaB, but rather than being an inhibitor it appears to function to stimulate transcription. The degradation of IkappaB is confirmed by immunoblotting.Synonyms: I kappa B-alpha, I-kappa-B-alpha, IkB-alpha, IkappaBalpha, MAD3, Major histocompatibility complex enhancer-binding protein MAD3, NF-kappa-B inhibitor alpha, NFKBI

ID gène: 4792

NCBI Accession: NP_065390

UniProt: P25963

Pathways: Signalisation NF-kappaB, TCR Signaling, Signalisation TLR, Fc-epsilon Receptor Signaling Pathway, Activation of Innate immune Response, Cellular Response to Molecule of Bacterial Origin, Maintenance of Protein Location, Hepatitis C, Protein targeting to Nucleus, Toll-Like Receptors Cascades, BCR Signaling