| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | CARD carrying kinase; CARD3; CARDIAK; CCK; CLARP kinase; GIG30; Growth inhibiting gene 30; Receptor interacting protein 2; RICK; RIP 2; Ripk2; TNFRSF;;RIP 2 |
| WB Predicted band size | 61 kDa |
| Host/Isotype | Rabbit IgG |
| 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 |
| Immunogen | A synthesized peptide derived from human RIP 2 |
| Formulation | Purified antibody in PBS with 0.05% sodium azide,0.05% BSA and 50% glycerol. |
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以下是3篇关于RIP2抗体的参考文献及其简要摘要：
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1. **文献名称**: *Nod2-dependent regulation of innate and adaptive immunity in the intestinal tract*
**作者**: Inohara, N. et al. (2003)
**摘要**: 研究通过使用RIP2特异性抗体，揭示了RIP2在NOD2信号通路中的核心作用，证明其通过激活NF-κB和MAPK通路介导肠道免疫应答，并参与克罗恩病等炎症性肠病的发病机制。
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2. **文献名称**: *CARD9 signaling in the innate immune response*
**作者**: Hsu, Y.M. et al. (2007)
**摘要**: 研究利用RIP2抗体进行免疫共沉淀实验，发现RIP2与CARD9蛋白相互作用，协同调控真菌感染中宿主免疫反应，表明RIP2是模式识别受体下游的关键衔接分子。
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3. **文献名称**: *RIP2 promotes inflammation and autoimmunity through kinase-dependent and kinase-independent mechanisms*
**作者**: Pellegrini, E. et al. (2017)
**摘要**: 通过Western blot和基因敲除模型结合RIP2抗体，证明RIP2不仅依赖激酶活性促进炎症(如IL-1β分泌)，还可通过构象改变参与自身免疫疾病(如类风湿性关节炎)的发生。
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4. **文献名称**: *Reciprocal modulation of Toll-like receptor-4 signaling pathways involving MyD88 and RIP2*
**作者**: Kobayashi, K. et al. (2005)
**摘要**: 研究通过抗体阻断实验，发现RIP2与TLR4信号通路存在交叉调控，提示其在天然免疫与获得性免疫间的桥梁作用，尤其在细菌脂多糖(LPS)诱导的炎症反应中至关重要。
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以上文献均涉及RIP2抗体的实验应用，涵盖其在先天免疫、疾病机制及信号通路解析中的关键作用。
The RIP2 (Receptor-Interacting Protein 2) antibody is a key tool for studying RIP2. a serine/threonine kinase also known as RIPK2 or CARD3. RIP2 plays a critical role in innate and adaptive immune signaling, primarily through its interaction with nucleotide-binding oligomerization domain (NOD) receptors, NOD1 and NOD2. Upon detection of bacterial components (e.g., peptidoglycans), these receptors recruit RIP2 via caspase recruitment domain (CARD)-mediated interactions, activating downstream NF-κB and MAPK pathways to trigger inflammatory responses. Dysregulation of RIP2 is linked to autoimmune diseases, chronic inflammation, and cancer.
RIP2 antibodies are widely used in techniques like Western blotting, immunoprecipitation, and immunofluorescence to detect RIP2 expression, post-translational modifications (e.g., ubiquitination), and subcellular localization. They help elucidate RIP2’s role in signaling crosstalk, including its crosstalk with TLR and TNF receptor pathways. Researchers also utilize these antibodies to explore RIP2 inhibition as a therapeutic strategy in conditions like inflammatory bowel disease, rheumatoid arthritis, and sepsis.
As RIP2-deficient models show impaired immune responses, the antibody aids in validating genetic models and assessing tissue-specific RIP2 expression. Its relevance in both infectious and sterile inflammation underscores its importance in immunology and drug development research.
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