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Anti-NFKB p105 (RABBIT) Antibody
NFkB p105 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Host | Rabbit |
|---|---|
| Conjugate | Unconjugated |
| Target Species | Human |
| Reactivity | Human |
| Clonality | Polyclonal |
Application 
| WB, E, I, LCI |
| Application Note | This product was assayed by immunoblot and found to be reactive against Human NFkB p105 at a dilution of 1:1000 followed by reaction with Peroxidase conjugated Affinity Purified anti-Rabbit IgG [H&L] (Goat) code #611-1302. See also Rockland Immunochemical's anti-Human NFkB p50 (NFKB1), which is suitable for the detection by immunoblot of both human NFkB p50 (NFKB1) and its precursor protein p105. |
| Physical State | Liquid (sterile filtered) |
| Immunogen | Human NFkB p105 peptide corresponding to a region near the N-terminus of the human protein conjugated to Keyhole Limpet Hemocyanin (KLH). |
| Preservative | 0.01% (w/v) Sodium Azide |
| Gene ID | 4790 |
|---|---|
| Other Names | 4790 |
| Purity | This product was prepared from monospecific antiserum by delipidation and defibrination. Anti-Human NFkB p105 may react non-specifically with other proteins. |
| Storage Condition | Store vial at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use. |
| Precautions Note | This product is for research use only and is not intended for therapeutic or diagnostic applications. |
| Name | NFKB1 |
|---|---|
| Function | NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-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 and the heterodimeric p65-p50 complex appears to be most abundant one. 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-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-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-kappa-B complex which translocates to the nucleus. NF-kappa-B heterodimeric p65-p50 and RelB-p50 complexes are transcriptional activators. The NF-kappa-B p50-p50 homodimer is a transcriptional repressor, but can act as a transcriptional activator when associated with BCL3. NFKB1 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p105 and generation of p50 by a cotranslational processing. The proteasome-mediated process ensures the production of both p50 and p105 and preserves their independent function, although processing of NFKB1/p105 also appears to occur post-translationally. p50 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. In a complex with MAP3K8, NFKB1/p105 represses MAP3K8-induced MAPK signaling; active MAP3K8 is released by proteasome-dependent degradation of NFKB1/p105. |
| Cellular Location | [Nuclear factor NF-kappa-B p105 subunit]: Cytoplasm |
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Provided below are standard protocols that you may find useful for product applications.
Background
NFkB was originally identified as a factor that binds to the immunoglobulin kappa light chain enhancer in B cells. It was subsequently found in non-B cells in an inactive cytoplasmic form consisting of NFkB bound to IkB. NFkB was originally identified as a heterodimeric DNA binding protein complex consisting of p65 (RelA) and p50 (NFKB1) subunits. Other identified subunits include p52 (NFKB2), c-Rel, and RelB. The p65, cRel, and RelB subunits are responsible for transactivation. The p50 and p52 subunits possess DNA binding activity but limited ability to transactivate. p52 has been reported to form transcriptionally active heterodimers with the NFkB subunit p65, similar to p50/p65 heterodimers. Both p50 and p52 are synthesized in a precursor form referred to as p105 and p100, respectively. The heterodimers of p52/p65 and p50/p65 are regulated by physical inactivation in the cytoplasm by an inhibitor called IkB-a. IkB-a binds to the p65 subunit, preventing nuclear localization and DNA binding. Low levels of p52 and p50 homodimers can also exist in cells. Reports describe the 607 aa C-terminal region (CTR) of p105 as IkB-g in that the molecule acts as an inhibitor of NFkB by binding to p65 and other NFkB subunits. p105 contains an N-terminal p50 domain followed by a glycine rich region (GRR), ankyrin repeat domain (ARD), death domain (DD) and destruction box (DB).
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