| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/100-1/300 | Human,Mouse,Rat |
| ICC | 1/200-1/1000 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/20000 | Human,Mouse,Rat |
| Aliases | TNFSF12; APO3L; DR3LG; Tumor necrosis factor ligand superfamily member 12; APO3 ligand; TNF-related weak inducer of apoptosis; TWEAK |
| Entrez GeneID | 407977;8742; |
| WB Predicted band size | 27kDa |
| 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,Mouse |
| Immunogen | Synthesized peptide derived from the Internal region of human TWEAK. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide,0.5%BSA and 50% glycerol. |
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以下是关于TWEAK抗体的3篇代表性文献，涵盖机制研究及治疗应用：
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1. **标题**：*TWEAK/Fn14 signaling in inflammation and tissue damage*
**作者**：Burkly LC, et al.
**摘要**：该综述系统阐述了TWEAK与其受体Fn14的相互作用在炎症反应、组织修复和纤维化中的作用，提出靶向TWEAK抗体可能通过调控巨噬细胞活性和细胞外基质重塑治疗自身免疫性疾病(如红斑狼疮)和慢性肾病。
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2. **标题**：*Anti-TWEAK monoclonal antibodies reduce immune cell infiltration and improve survival in a murine lupus nephritis model*
**作者**：Zhao Z, et al.
**摘要**：研究团队开发了一种靶向TWEAK的单克隆抗体，并在狼疮肾炎小鼠模型中验证其疗效。结果显示，抗体治疗显著减少肾脏中T细胞和巨噬细胞浸润，降低蛋白尿水平，并通过抑制NF-κB通路延缓疾病进展。
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3. **标题**：*TWEAK inhibition restores endothelial function in experimental atherosclerosis*
**作者**：Novoyatleva T, et al.
**摘要**：该研究证明TWEAK抗体可改善动脉粥样硬化模型中的内皮功能障碍。机制上，抗体通过阻断TWEAK诱导的氧化应激和VCAM-1表达，恢复血管内皮细胞的NO生物利用度，提示其在心血管疾病中的潜在应用价值。
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**领域覆盖**：上述文献分别从基础机制(炎症调控)、疾病模型(狼疮肾炎)和血管病变(动脉粥样硬化)三个维度解析TWEAK抗体的作用，涉及单抗开发、信号通路验证及临床前疗效评估。如需补充特定疾病方向文献可进一步说明。
TWEAK (TNF-like weak inducer of apoptosis) is a multifunctional cytokine belonging to the tumor necrosis factor (TNF) superfamily. Initially identified in 1997. it interacts with its sole receptor, Fn14 (fibroblast growth factor-inducible 14), to regulate cellular processes including proliferation, apoptosis, inflammation, and tissue remodeling. Structurally, TWEAK is a type II transmembrane protein that can be proteolytically cleaved to release a soluble form. Its signaling activates multiple pathways, such as NF-κB, MAPK, and AKT, influencing both physiological and pathological conditions.
TWEAK/Fn14 signaling is implicated in diverse diseases, including cancer, autoimmune disorders, atherosclerosis, and neurodegenerative diseases. In cancer, it promotes tumor growth, angiogenesis, and metastasis, while in chronic inflammatory conditions like lupus or rheumatoid arthritis, it exacerbates tissue damage. Conversely, TWEAK also exhibits protective roles in tissue repair and regeneration, highlighting its context-dependent duality.
TWEAK antibodies, designed to block TWEAK-Fn14 interactions, have emerged as therapeutic tools. Preclinical studies show their potential to inhibit tumor progression, reduce inflammation in autoimmune models, and mitigate fibrosis. Clinical trials are exploring their efficacy in conditions like multiple sclerosis and kidney fibrosis. Despite challenges in balancing therapeutic benefits with off-target effects, TWEAK antibodies represent a promising avenue for targeting pathways central to inflammation and tissue injury.
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