Mouse V-Rel Reticuloendotheliosis Viral Oncogene Homolog B (RELB) Protein
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Description
Recombinant V-Rel Reticuloendotheliosis Viral Oncogene Homolog B (RELB) is a recombinant Mouse protein produced in a Prokaryotic expression system (E. coli).
Documents del producto
Product specifications
| Category | Proteins and Peptides |
| Immunogen Target | V-Rel Reticuloendotheliosis Viral Oncogene Homolog B (RELB) |
| Host | E. coli |
| Origin | Mouse |
| Conjugation | Unconjugated |
| Observed MW | Molecular Weight: Calculated MW: 33.3 kDa Observed MW (SDS-PAGE): 33 kDa Concentration: Prior to lyophilization: 200 µg/ml Sequence Fragment: Leu176-Ser436 Tag: N-terminal His tag |
| Expression | Recombinant |
| Purity | > 95% |
| Size 1 | 10 µg |
| Size 2 | 50 µg |
| Size 3 | 100 µg |
| Size 4 | 200 µg |
| Size 5 | 500 µg |
| Form | Lyophilized To keep the original salt concentration, we recommend reconstituting to the original concentration prior to lyophilization (see Concentration) in ddH2O. If a lower concentration is required, dilute in PBS, pH 7.4. If a higher concentration is required, the product can be reconstituted directly in PBS, pH 7.4, though please note that this will change the overall salt concentration. The stock concentration should be between 0.1-1.0 mg/ml. Do not vortex. |
| Tested Applications | WB, SDS-PAGE |
| Buffer | Prior to lyophilization: PBS, pH 7.4, containing 0.01% Sarcosyl, 1 mM DTT, 5% Trehalose and Proclin-300. |
| Availability | Shipped within 5-7 working days. |
| Storage | Store at 2-8 °C for up to one month. Store at -80 °C for up to one year. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | Q04863 |
| Background | Protein RELB |
| Status | RUO |
| Note | This product is for research use only. Not for human consumption, cosmetic, therapeutic or diagnostic use. |
Descripción
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NF-kappa-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-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. 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 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. As a member of the NUPR1/RELB/IER3 survival pathway, may provide pancreatic ductal adenocarcinoma with remarkable resistance to cell stress, such as starvation or gemcitabine treatment. Regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-ARNTL/BMAL1 heterodimer in a CRY1/CRY2 independent manner. Increased repression of the heterodimer is seen in the presence of NFKB2/p52.
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NF-kappa-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-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. 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 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. As a member of the NUPR1/RELB/IER3 survival pathway, may provide pancreatic ductal adenocarcinoma with remarkable resistance to cell stress, such as starvation or gemcitabine treatment. Regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-ARNTL/BMAL1 heterodimer in a CRY1/CRY2 independent manner. Increased repression of the heterodimer is seen in the presence of NFKB2/p52.
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