| WB | 1/500-1/1000 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/50-1/100 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 1/50-1/100 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | FADD protein; GIG3; Growth inhibiting gene 3 protein; Mediator of receptor induced toxicity; MORT1 |
| Entrez GeneID | 14082 |
| WB Predicted band size | Calculated MW: 23 kDa; Observed MW: 28 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 | Mouse |
| Immunogen | A synthesized peptide derived from mouse FADD |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
+ +
以下是3篇与FADD抗体相关的参考文献及其摘要概括：
---
1. **文献名称**：*FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis*
**作者**：Chinnaiyan AM, et al.
**摘要**：该研究首次鉴定了FADD蛋白(Fas-associated death domain)，揭示了其通过死亡结构域与Fas受体结合，并激活caspase-8依赖的凋亡信号通路。实验中使用FADD抗体验证了其在凋亡复合体中的关键作用，为死亡受体信号机制奠定了基础。
---
2. **文献名称**：*Targeted disruption of the FADD gene results in early embryonic lethality*
**作者**：Yeh WC, et al.
**摘要**：通过基因敲除技术发现FADD缺失导致小鼠胚胎早期死亡，证明FADD不仅是凋亡通路的核心分子，还参与胚胎发育调控。研究利用FADD抗体进行组织特异性表达分析，强调了其在免疫系统及发育中的双重功能。
---
3. **文献名称**：*FADD regulates NF-κB activation and promotes ubiquitination of caspase-8 and RIPK1 in TNF signalling*
**作者**：Lavrik IN, et al.
**摘要**：研究发现FADD通过调控TNF信号中RIPK1和caspase-8的泛素化，影响NF-κB激活和细胞存活/凋亡平衡。通过FADD抗体的免疫共沉淀实验，揭示了其与复合体II的动态互作机制，为炎症与癌症治疗提供新靶点。
---
4. **文献名称**：*The role of FADD in necroptosis and viral infection*
**作者**：He S, et al.
**摘要**：本文探讨FADD在坏死性凋亡(necroptosis)中的作用，发现FADD缺失细胞对病毒感染的敏感性增加。通过FADD抗体阻断实验，证实其与RIPK3/MLKL通路的交叉调控，扩展了FADD在非经典死亡途径中的功能认知。
---
这些文献覆盖了FADD在凋亡、发育、炎症及坏死性凋亡中的核心机制，实验方法均涉及FADD抗体的应用(如Western blot、免疫共沉淀等)，可作为相关研究的关键参考。
**Background of FADD Antibody**
FADD (Fas-associated protein with death domain) is a critical adaptor protein involved in apoptosis (programmed cell death) and inflammatory signaling pathways. It contains a C-terminal death domain (DD) and an N-terminal death effector domain (DED), enabling interactions with death receptors (e.g., Fas, TRAIL receptors) and initiator caspases (e.g., caspase-8/10). FADD bridges receptor-ligand binding to caspase activation, triggering the extrinsic apoptosis pathway. Dysregulation of FADD is linked to cancer, autoimmune disorders, and neurodegenerative diseases.
FADD antibodies are essential tools for studying its expression, localization, and function. They are used in techniques like Western blot, immunohistochemistry (IHC), and flow cytometry to detect FADD levels in tissues or cells. Researchers employ these antibodies to explore mechanisms of apoptosis resistance in tumors or aberrant immune activation. Notably, FADD phosphorylation (e.g., at Ser194 in humans) modulates its activity, and specific antibodies can distinguish phosphorylated forms.
Discrepancies in FADD’s role (e.g., pro-survival vs. pro-apoptotic effects in certain cancers) highlight its context-dependent functions. Antibodies aid in clarifying these dual roles, supporting drug discovery and biomarker studies. Commercial FADD antibodies are typically validated for specificity across species (human, mouse, rat), ensuring reliability in diverse experimental models. Their applications extend to studying necroptosis and autophagy, underscoring FADD’s versatility in cell fate regulation.
×
