癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
C-rel (NFkB) Antibody (C-term)
Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, E |
|---|---|
| Primary Accession | Q04864 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 68520 Da |
| Antigen Region | 586-619 aa |
| Gene ID | 5966 |
|---|---|
| Other Names | Proto-oncogene c-Rel, REL |
| Target/Specificity | This C-rel (NFkB) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 586-619 amino acids from the C-terminal region of human C-rel (NFkB). |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | C-rel (NFkB) Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | REL |
|---|---|
| Function | Proto-oncogene that may play a role in differentiation and lymphopoiesis. 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. The NF-kappa-B heterodimer RELA/p65- c-Rel is a transcriptional activator. |
| Cellular Location | Nucleus. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Nuclear factor (NF)-kappa B is a sequence specific transcriptional activator that binds to the intronic enhancer of kappa light chain gene in B lymphocytes. NF-kB regulates the expression of a wide variety of genes that involved in apoptosis, viral life cycle, tumorigenesis, autoimmune diseases and inflammation. NF-kB is a heterodimer of members of the rel family of proteins such as p50, p65, and c-rel. In most cells, inhibitory IkB proteins sequester NF-kB/Rel in the cytoplasm. Cellular stimulation precipitates degradation of IkB and modification of NF-kB/Rel proteins, permitting translocation of NF-kB/Rel (c-Rel and RelA) to the nucleus for action on target genes. The important role of c-Rel in B-cell development, growth, and survival has been intensively studied, as well as its function in differentiation and lymphopoiesis (particularly lymphoid cancer).
REFERENCES
Jain, A., et al., J. Clin. Invest. 114(11):1593-1602 (2004).
Xiao, Q., et al., Appl. Immunohistochem. Mol. Morphol. 12(3):211-215 (2004).
Houldsworth, J., et al., Blood 103(5):1862-1868 (2004).
Phelps, C.B., et al., Oncogene 23(6):1229-1238 (2004).
Bernard, D., et al., Cancer Res. 64(2):472-481 (2004).
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