| WB | 1/500 - 1/2000 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/100 - 1/500 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/10000 | Human,Mouse,Rat |
| Aliases | NFkappaB p65; p65; NFKB3; RELA |
| Entrez GeneID | 5970 |
| clone | 6H7 |
| WB Predicted band size | 65kDa |
| Host/Isotype | Mouse IgG1 |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human,Mouse,Rat,Rabbit,Monkey |
| Immunogen | Purified recombinant fragment of human NF-κB p65 expressed in E. Coli. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于NF-κB p65抗体的3篇参考文献示例(基于经典研究，内容为模拟概括)：
1. **文献名称**：*"NF-κB p65 phosphorylation at serine 536 is essential for the induction of pro-inflammatory cytokines in macrophages"*
**作者**：Chen L, Fischle W, Verdin E, et al.
**摘要**：研究通过Western blot和免疫荧光技术，使用p65特异性抗体分析了巨噬细胞中p65磷酸化位点(Ser536)对炎症因子表达的调控机制。
2. **文献名称**：*"Selective inhibition of NF-κB activation by a peptide that blocks the interaction of TAK1 with the IκB kinase complex"*
**作者**：Karin M, Yamamoto Y, Wang QM.
**摘要**：通过免疫共沉淀(Co-IP)和ChIP实验，结合p65抗体，揭示了TAK1激酶在NF-κB信号通路中激活p65的关键作用及药物干预靶点。
3. **文献名称**：*"Chromatin-specific regulation of NF-κB by histone modifications in human breast cancer cells"*
**作者**：Perkins ND, Gilmore TD.
**摘要**：利用p65抗体进行染色质免疫沉淀测序(ChIP-seq)，阐明了组蛋白修饰与p65在乳腺癌细胞中的转录调控关联。
4. **文献名称**：*"A critical role for the RelA subunit of NF-κB in TLR4-induced gene expression"*
**作者**：Kawai T, Akira S.
**摘要**：通过基因敲除模型和p65抗体介导的凝胶迁移实验(EMSA)，证实RelA/p65在TLR4信号通路中调控炎症基因的核心功能。
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如需具体文献，建议通过PubMed或Google Scholar检索关键词“NF-κB p65 antibody”+应用技术(如Western blot/ChIP)，并筛选近年的高引论文。
The NF-κB p65 antibody is a critical tool for studying the NF-κB signaling pathway, a central regulator of immune responses, inflammation, cell survival, and proliferation. NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells) comprises a family of transcription factors, with p65 (RelA) being a key subunit of the canonical pathway. The p65 protein forms heterodimers with p50. which translocate to the nucleus upon activation to regulate target gene expression. Antibodies targeting p65 are widely used to detect its expression, localization, and activation status in experimental models.
In resting cells, NF-κB p65 is sequestered in the cytoplasm by inhibitory proteins like IκB. Pro-inflammatory stimuli (e.g., cytokines, pathogens) trigger IκB degradation via the IKK complex, allowing p65 nuclear translocation. Researchers employ p65 antibodies in techniques such as Western blotting, immunofluorescence, and chromatin immunoprecipitation (ChIP) to assess pathway activation. These antibodies help elucidate NF-κB's role in diseases, including cancer, autoimmune disorders, and chronic inflammation.
Specificity and validation are crucial, as cross-reactivity with other Rel family members (e.g., RelB, c-Rel) can occur. Anti-p65 antibodies are often raised in rabbits or mice against epitopes within the N-terminal Rel homology domain or C-terminal transactivation domain. Their applications span basic research, drug development (e.g., testing NF-κB inhibitors), and clinical biomarker studies, making them indispensable for dissecting inflammatory and oncogenic mechanisms.
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