| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 1/100-1/200 | Human,Mouse,Rat |
| IHC | 1/100-1/200 | 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 |
| Host/Isotype | Mouse IgG2b |
| 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 | Purified recombinant fragment of human DGKZ |
| Formulation | Purified antibody in PBS with 0.05% sodium azide |
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以下是关于DGKZ抗体的3篇参考文献示例(注：文献为模拟生成，仅供参考)：
1. **标题**：*DGKζ regulates T-cell receptor signaling by modulating diacylglycerol turnover*
**作者**：Sanjabi S, et al.
**摘要**：该研究利用DGKZ特异性抗体，发现DGKζ通过降解二酰基甘油(DAG)负调控T细胞受体信号通路，影响T细胞活化及免疫应答，为自身免疫疾病治疗提供新靶点。
2. **标题**：*Elevated DGKZ expression correlates with poor prognosis in hepatocellular carcinoma*
**作者**：Li Y, Wang X, Zhang H.
**摘要**：通过免疫组化(使用DGKZ抗体)分析肝癌组织，发现DGKZ高表达与肿瘤转移及患者生存期缩短显著相关，提示其可作为肝癌预后生物标志物。
3. **标题**：*DGKζ deficiency alters synaptic plasticity via mTOR pathway dysregulation*
**作者**：Martinez E, et al.
**摘要**：研究采用DGKZ敲除小鼠及Western blot(基于DGKZ抗体)证实，DGKζ缺失导致海马区突触可塑性异常，可能与mTOR信号失调有关，为神经退行性疾病机制提供新见解。
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如需真实文献，建议通过PubMed或Google Scholar以“DGKZ antibody”或“diacylglycerol kinase zeta”为关键词检索近年研究。
DGKZ (diacylglycerol kinase zeta) is a member of the diacylglycerol kinase (DGK) family, which comprises enzymes that phosphorylate diacylglycerol (DAG) to generate phosphatidic acid (PA). These lipid mediators play critical roles in cellular signaling, influencing processes like proliferation, apoptosis, and membrane trafficking. DGKZ, specifically, is a type II DGK isoform localized predominantly in the nucleus and cytoplasm, with expression observed in immune cells, neurons, and various tissues. It contains a pleckstrin homology (PH) domain, nuclear localization signals, and a sterile alpha motif (SAM), which regulate its subcellular localization and interactions.
Research highlights DGKZ's involvement in immune regulation, particularly in T-cell receptor signaling. By converting DAG to PA, DGKZ modulates downstream pathways, including Ras/ERK and mTOR, affecting T-cell activation, anergy, and differentiation. Dysregulation of DGKZ has been linked to autoimmune diseases, cancer, and neurological disorders. For instance, reduced DGKZ activity may enhance T-cell responses, contributing to autoimmunity, while its overexpression in cancers may promote survival signaling.
DGKZ antibodies are essential tools for detecting protein expression, phosphorylation states, and subcellular distribution in experimental models. They enable studies exploring DGKZ's role in lipid signaling, immune dysfunction, and disease mechanisms, aiding therapeutic target identification. Commercial antibodies are typically validated for techniques like Western blot, immunofluorescence, and immunohistochemistry, though cross-reactivity with other DGK isoforms remains a consideration.
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