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- 详细信息
- 技术资料
- 抗体英文名:
RIP Antibody
- 抗原:
synthetic peptide corresponding to residues surrounding arginine 413 of human RIP
- 应用范围:
W
- 宿主:
Rabbit
- 级别:
详见MSDS文件
- 适应物种:
H,Mk
- 供应商:
CST
- 保质期:
详见说明书
- 库存:
大量
- 是否单克隆:
2
- 保存条件:
-20°c
- 规格:
100 ul (10 western blots)/carrier free & custom formulation / quantity
| 规格: | 产品价格: | ¥请询价 | |
|---|---|---|---|
| 规格: | 100 ul (10 western blots) | 产品价格: | ¥请询价 |
| 规格: | carrier free & custom formulation / quantity | 产品价格: | ¥请询价 |
pathway more info application references datasheet PDF MSDS PDF protocols
Applications Key: W=Western Blotting
Reactivity Key: H=Human Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
| Applications | Reactivity | Sensitivity | MW (kDa) | Source |
|---|---|---|---|---|
| W | H Mk | Endogenous | 78 | Rabbit |
| Protocols |
|
|---|---|
| Specificity / Sensitivity | RIP Antibody detects endogenous levels of RIP (RIP1) protein. No cross-reactivity was detected with other family members. This antibody also detects a carboxy-terminal fragment of RIP (45 kDa) produced by caspase-8 dependent cleavage. |
| Source / Purification | Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding arginine 413 of human RIP. Antibodies were purified by protein A and peptide affinity chromatography. |
| Background | The RIP (receptor-interacting protein) family of serine-threonine kinases (RIP, RIP2, RIP3 and RIP4) are important regulators of cellular stress that can trigger pro-survival and inflammatory responses through the activation of NF-κB as well as pro-apoptotic pathways (1). In addition to the kinase domain, RIP contains a death domain responsible for interaction with the death domain receptor Fas and for the recruitment to TNFR1 through interaction with TRADD (2,3). RIP also interacts with TNF-receptor-associated factors (TRAFs) and can recruit IKKs to the TNFR1 signaling complex via interaction with NEMO leading to IκB phosphorylation and degradation (6,7). Overexpression of RIP induces both NF-κB activation and apoptosis (2,3). Caspase-8 dependent cleavage of the death domain on RIP can trigger the apoptotic activity of RIP (8). RIP-deficient cells show a failure in TNF-mediated NF-κB activation making the cells more sensitive to apoptosis (4,5).
|
| Application References | Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know ! |
| Companion Products |
For Research Use Only. Not For Use In Diagnostic Procedures. |
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