RIP Antibody

• 产品编号：CST-4926S      品牌：CST       原厂货号：4926S
• 产品分类：抗体 > 一抗 > 蛋白特异性一抗
• 应用分类：

描述：

RIP 抗体能够检测内源水平RIP (RIP1)蛋白。此抗体不与其它家族的成员交叉反应。此抗体也能检测到caspase-8依赖剪切的45 kDa RIP蛋白C-末端片段。此多克隆抗体是通过合成人源对应的RIP Arg413位点周围的肽段来免疫动物而获得。抗体是通过protein A和多肽亲和层析纯化。RIP (受体互作蛋白)家族丝氨酸-苏氨酸激酶(RIP, RIP2, RIP3 and RIP4)是细胞胁迫的重要调控因子，它能够通过NF-κB信号通路和促凋亡通路而引起存活和炎症反应(1)。除了激酶区域, RIP也包含了死亡域，它能够死亡域受体Fas相互作用并通过与TRADD的相互作用招募到TNFR1上(2,3)。RIP也与TNF受体相关的因子(TRAFs)并且通过与NEMO的相互作用招募IKKs到TNFR1信号复合体上从而引起IκB的磷酸化及降解(6,7)。过表达RIP能够诱导NF-κB的激活和凋亡(2,3)。Caspase-8依赖的对RIP死亡域的剪切能引起其凋亡活性(8)。RIP缺失的细胞在TNF介导的NF-κB激活从而引起细胞对凋亡更为敏感方面的功能缺失(4,5)。

1. Meylan, E. and Tschopp, J. (2005) Trends Biochem Sci 30, 151-9.
2. Hsu, H. et al. (1996) Immunity 4, 387-96.
3. Stanger, B.Z. et al. (1995) Cell 81, 513-23.
4. Ting, A.T. et al. (1996) EMBO J 15, 6189-96.
5. Kelliher, M.A. et al. (1998) Immunity 8, 297-303.
6. Devin, A. et al. (2000) Immunity 12, 419-29.
7. Zhang, S.Q. et al. (2000) Immunity 12, 301-11.
8. Lin, Y. et al. (1999) Genes Dev 13, 2514-26.

原厂资料：

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).

1. Meylan, E. and Tschopp, J. (2005) Trends Biochem Sci 30, 151-9.
2. Hsu, H. et al. (1996) Immunity 4, 387-96.
3. Stanger, B.Z. et al. (1995) Cell 81, 513-23.
4. Ting, A.T. et al. (1996) EMBO J 15, 6189-96.
5. Kelliher, M.A. et al. (1998) Immunity 8, 297-303.
6. Devin, A. et al. (2000) Immunity 12, 419-29.
7. Zhang, S.Q. et al. (2000) Immunity 12, 301-11.
8. Lin, Y. et al. (1999) Genes Dev 13, 2514-26.

注意事项：

Storage: Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM
NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C.
Do not aliquot the antibody.