| WB | 咨询技术 | 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 | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | TNFRSF10D; DCR2; TRAILR4; TRUNDD; Tumor necrosis factor receptor superfamily member 10D; Decoy receptor 2; DcR2; TNF-related apoptosis-inducing ligand receptor 4; TRAIL receptor 4; TRAIL-R4; TRAIL receptor with a truncated death domain; CD |
| Entrez GeneID | 8793 |
| WB Predicted band size | Calculated MW: 42 kDa; Observed MW: 35 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 | Human |
| Immunogen | A synthetic peptide of human DcR2 |
| Formulation | Purified antibody in TBS with 0.05% sodium azide,0.05%BSA and 50% glycerol. |
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以下是3-4条关于DcR2抗体的参考文献示例(内容为虚构，供参考)：
1. **标题**: "DcR2 Expression in Tumor Cells Modulates Apoptosis Resistance via TRAIL Pathway Inhibition"
**作者**: Smith A, et al.
**期刊/年份**: *Cancer Research* (2003)
**摘要**: 研究通过免疫组化分析发现，DcR2在多种肿瘤细胞中高表达，并通过竞争性结合TRAIL配体抑制凋亡信号，提示其与肿瘤耐药性相关。
2. **标题**: "DcR2 Antibody Blockade Enhances Chemotherapy Sensitivity in Colorectal Cancer Models"
**作者**: Johnson R, et al.
**期刊/年份**: *Cell Death & Disease* (2015)
**摘要**: 开发靶向DcR2的单克隆抗体，实验表明其可逆转肿瘤细胞对化疗药物的耐药性，机制与恢复TRAIL介导的caspase激活有关。
3. **标题**: "DcR2 Regulates Inflammatory Signaling in Macrophages via NF-κB Activation"
**作者**: Lee S, et al.
**期刊/年份**: *Journal of Immunology* (2018)
**摘要**: 利用DcR2特异性抗体阻断实验，揭示DcR2通过调控NF-κB通路促进巨噬细胞炎症因子释放，为自身免疫疾病治疗提供新靶点。
4. **标题**: "A Novel Anti-DcR2 Antibody-Payload Conjugate for Targeted Cancer Therapy"
**作者**: Chen X, et al.
**期刊/年份**: *Nature Communications* (2022)
**摘要**: 报道一种新型DcR2抗体-药物偶联物(ADC)，在临床前模型中显著抑制实体瘤生长，且对正常组织毒性较低。
(注：以上文献为模拟示例，实际引用需查询真实数据库如PubMed、Web of Science等。)
DcR2 (Decoy Receptor 2), also known as TNFRSF10D or TRAIL-R4. is a member of the tumor necrosis factor (TNF) receptor superfamily. Unlike its pro-apoptotic counterparts TRAIL-R1 (DR4) and TRAIL-R2 (DR5), DcR2 lacks a functional death domain and instead contains a truncated cytoplasmic domain, rendering it incapable of initiating apoptosis. It acts as a decoy receptor by binding to TRAIL (TNF-related apoptosis-inducing ligand), thereby competitively inhibiting TRAIL-induced apoptosis. This regulatory mechanism helps protect normal cells from unintended cell death while modulating immune responses.
DcR2 is broadly expressed in healthy tissues but is frequently overexpressed in various cancers, including colorectal, lung, and breast cancers. Its upregulation in tumors is associated with resistance to apoptosis, promoting cancer cell survival and therapeutic resistance. DcR2 antibodies are critical tools for studying its role in cancer biology, enabling detection of protein expression, functional blocking experiments, and exploration of its interplay with apoptotic pathways. Research on DcR2-targeting antibodies also explores their therapeutic potential, either as standalone agents or in combination with TRAIL-based therapies to overcome cancer resistance mechanisms. Understanding DcR2's dual role in physiological homeostasis and pathological evasion of cell death remains a key focus in oncology and immunology research.
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