RelB (Ab 573) Antibody | 79-595

RelB (Ab 573) Antibody | 79-595 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse

Homology: N/A

Immunogen: RelB (Ab-573) antibody was raised against a peptide sequence around aa. 550~554 (L-L-S-P-G) derived from Human RelB.

Research Area: Other

Tested Application: WB

Application: Western Blot: 1:500~1:1000

Specificiy: This antibody detects endogenous level of total RelB protein.

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 70 kDa

Validation: N/A

Isoform: N/A

Purification: Antibodies were purified by affinity-chromatography using epitope-specific peptide.

Clonality: Polyclonal

Clone: N/A

Isotype: N/A

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Antibody supplied in phosphate buffered saline (without Mg2+ and Ca2+) , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

Concentration: 1 mg/mL

Storage Condition: Store antibody at -20˚C for up to one year.

Alternate Name: IREL, I-REL, REL-B, NFKB3, I-Rel

User Note: N/A

BACKGROUND: NF-κ-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-κ-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-κ-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-κ-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-κ-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-κ-B complex which translocates to the nucleus. NF-κ-B heterodimeric RelB-p50 and RelB-p52 complexes are transcriptional activators. RELB neither associates with DNA nor with RELA/p65 or REL. Stimulates promoter activity in the presence of NFKB2/p49.