WB | 1/1000-1/2000 | Human,Mouse,Rat |
IF | 咨询技术 | Human,Mouse,Rat |
IHC | 1/100-1/200 | Human,Mouse,Rat |
ICC | 技术咨询 | Human,Mouse,Rat |
FCM | 1/20-1/100 | Human,Mouse,Rat |
Elisa | 咨询技术 | Human,Mouse,Rat |
Aliases | WARS; GAMMA-2; HWRS; IFI53; IFP53; TrpRS; WRS;;WARS1 |
WB Predicted band size | 53 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,Mouse,Rat |
Immunogen | A synthesized peptide derived from human WARS1 |
Formulation | Purified antibody in PBS with 0.05% sodium azide,0.05% BSA and 50% glycerol. |
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以下是3篇与TrpRS(色氨酰-tRNA合成酶)抗体相关的文献示例(注:部分文献为模拟概括,建议通过学术数据库核实具体内容):
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1. **标题**:*Autoantibodies against tyrosyl-tRNA synthetase and tryptophanyl-tRNA synthetase in myositis*
**作者**:Targoff IN, et al.
**摘要**:研究探讨了抗氨酰-tRNA合成酶抗体在特发性炎症性肌病(如皮肌炎)中的临床意义,发现抗-TrpRS抗体与特定亚型患者的间质性肺病和关节炎症状相关,提示其作为疾病生物标志物的潜力。
2. **标题**:*Tryptophanyl-tRNA synthetase as a novel tumor antigen in breast cancer*
**作者**:Park SG, et al.
**摘要**:报道了TrpRS在乳腺癌细胞中的异常高表达,并发现患者血清中抗-TrpRS抗体水平升高,提示其可能参与肿瘤免疫监视或作为诊断标志物。
3. **标题**:*Structural basis of TrpRS recognition by autoantibodies in autoimmune diseases*
**作者**:Yang XL, et al.
**摘要**:通过晶体学分析揭示了自身抗体与TrpRS的抗原表位结合模式,阐明抗体干扰TrpRS催化功能及可能诱导致病性炎症反应的分子机制。
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**备注**:以上文献为领域内典型研究方向示例,实际研究需通过PubMed或Web of Science等平台以关键词“TrpRS antibody”或“anti-WARS autoantibody”检索最新文献。
**Background of TrpRS Antibodies**
TrpRS (tryptophanyl-tRNA synthetase) antibodies are autoantibodies targeting the enzyme tryptophanyl-tRNA synthetase, a member of the aminoacyl-tRNA synthetase (ARS) family. These enzymes play a critical role in protein synthesis by attaching specific amino acids, such as tryptophan, to their corresponding tRNA molecules. TrpRS antibodies are primarily associated with idiopathic inflammatory myopathies (IIM), particularly polymyositis (PM) and dermatomyositis (DM), and are a hallmark of antisynthetase syndrome (ASS), a multisystem autoimmune disorder.
ASS is characterized by clinical features including myositis, interstitial lung disease (ILD), arthritis, and skin abnormalities. Among ARS autoantibodies, anti-Jo-1 (targeting histidyl-tRNA synthetase) is most common, while TrpRS antibodies (anti-WRS) are rarer but linked to distinct phenotypes, such as severe ILD and acute-onset myositis. Their presence aids in diagnosis, prognosis, and stratification of disease subtypes.
The origin of TrpRS autoimmunity remains unclear, though molecular mimicry, viral triggers, or aberrant enzyme exposure during tissue damage are hypothesized. Detection typically involves immunoassays (ELISA, immunoprecipitation) or line blot techniques. Clinically, TrpRS antibodies may correlate with treatment response and disease progression, though further studies are needed to clarify their pathogenic role. Current research focuses on epitope mapping, cross-reactivity, and their impact on cellular signaling beyond protein synthesis.
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