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Rabbit Monoclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB |
|---|---|
| Primary Accession | Q61160 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Monoclonal |
| Clone Names | EPR1816Y |
| Calculated MW | 22960 Da |
| Gene ID | 14082 |
| Other Names | FAS-associated death domain protein, FAS-associating death domain-containing protein, Mediator of receptor induced toxicity, Protein FADD, Fadd, Mort1 |
| Target/Specificity | A synthetic peptide corresponding to residues surrounding serine 194 of human FADD was used as immunogen. |
| Dilution | WB~~1:500 |
| Format | 50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | FADD Antibody Phospho (pS194) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | Fadd |
|---|---|
| Synonyms | Mort1 |
| Function | Apoptotic adaptor molecule that recruits caspase-8 or caspase-10 to the activated Fas (CD95) or TNFR-1 receptors. The resulting aggregate called the death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation. Active caspase-8 initiates the subsequent cascade of caspases mediating apoptosis (By similarity). Involved in interferon-mediated antiviral immune response, playing a role in the positive regulation of interferon signaling (By similarity). |
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Provided below are standard protocols that you may find useful for product applications.
Background
Fas-associating protein with death domain (FADD) is an adaptor protein involved in the apoptosis induced by Fas and TNF-R1, and mitogen induced cell proliferation (1). FADD consists of death domain (DD) at the C-terminal and death effector domain (DED) at the N-terminal (2). DD interacts with Fas and TNF-R1, which exposes the DED portion on the FADD. Unmasked DED binds to the DED of pro-caspase-8, which activates the cysteine protease cascade (3). The development of autoimmune lymphoproliferative (lpr) diseases has been linked to inactivation of Fas-FADD interaction (4). Also, the deficiency in FADD can inhibit TRAIL-induced cell apoptosis. In cancer cells, higher phopsholyation of FADD at serine 194 is expressed compared to normal cells. Phospholyation at serine 194 has been linked to induction of apoptosis by anti-cancer drugs in human protstate cancer cells and it is considered as a valuable maker for human prostate cancer progression (5).
References
1. Imtiyaz HZ et al, I J. Biol. Chem., 280(36);31360-67, 2005
2. Chinnaiyan AM et al. Cell 81, 505
3. Boldin MP et al, Cell 85, 803
4. Cohen PL et al. Annu. Rev. Immunol. 9, 243
5. Shimada K, et al. J Pathol 206:423-32, 2005.
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