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Cell Signaling Phospho-Rip (Ser166) (E7g6o) Rabbit mAb
List Price $412.00 Your Price $412.00
Cell Signaling Phospho-Rip (Ser166) (E7g6o) Rabbit mAb - CSSPQ (Additional S&H or Hazmat Fees May Apply)
NETA PART: CSSPQ-53286S
MFG.PART: 53286S
UNSPSC: 12352203
Manufacturer: Cell Signaling
| Size | 100 µl |
| Reactivity | M R |
| Sensitivity | Endogenous |
| Molecular Weight (kDa) | 78 |
| Source/Isotype | Rabbit IgG |
| Application/Dilution | {Western Blotting: 1:1000, Immunoprecipitation: 1:100} |
| Storage | Supplied in 10 mm sodium HEPES (pH 7.5), 150 mm NaCl, 100 µg/mL BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody. |
| Specificity/Sensitivity | Phospho-RIP (Ser166) (E7G6O) Rabbit mAb recognizes endogenous levels of RIP protein only when phosphorylated at Ser166. |
| Species Reactivity | Mouse, Rat |
| Source/Purification | Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser166 of mouse RIP protein. |
| Background | The receptor-interacting protein (RIP) family of serine-threonine kinases (RIP, RIP2, RIP3, and RIP4) are important regulators of cellular stress that 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 recruitment to TNF-R1 through interaction with TRADD (2,3). RIP-deficient cells show a failure in TNF-mediated NF-κB activation, making the cells more sensitive to apoptosis (4,5). RIP also interacts with TNF-receptor-associated factors (TRAFs) and can recruit IKKs to the TNF-R1 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 RIP death domain can trigger the apoptotic activity of RIP (8).Necroptosis, a regulated pathway for necrotic cell death, is triggered by a number of inflammatory signals including cytokines in the tumor necrosis factor (TNF) family, pathogen sensors such as toll-like receptors (TLRs), and ischemic injury (9,10). The process is negatively regulated by caspases and is initiated through a complex containing the RIP and RIP3 kinases, typically referred to as the necrosome. Necroptosis is inhibited by a small molecule inhibitor of RIP, necrostatin-1 (Nec-1) (11). Research studies show that necroptosis contributes to a number of pathological conditions, and Nec-1 has been shown to provide neuroprotection in models such as ischemic brain injury (12). RIP is phosphorylated at several sites within the kinase domain that are sensitive to Nec-1, including Ser14, Ser15, Ser161, and Ser166 (13). |
| SKU | CSSPQ-53286S |
|---|---|
| Supplier Part Number | 53286S |
| UM | EA |
| UNSPSC | 12352203 |
| Manufacturer | Cell Signaling |
| MSDS URL | Click here |
| Temperature | -20C |
| CountryOfOrigin | United States |
| ProductLine | CSSPQ |
| Qty | 1 |
| MinOrderQty | 1 |
| Weight | 7.000000 |
| Lead Time | 5 |
| Hazardous | N |
| Energy Star | No |
| Green | No |
| Controlled | N |