| 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 | 1/50-1/200 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | CHEK2; CDS1; CHK2; RAD53; Serine/threonine-protein kinase Chk2; CHK2 checkpoint homolog; Cds1 homolog; Hucds1; hCds1; Checkpoint kinase 2 |
| Entrez GeneID | 11200 |
| WB Predicted band size | Calculated MW: 61 kDa; Observed MW: 61 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 | The antiserum was produced against synthesized peptide derived from human Chk2 around the phosphorylation site of Thr68. AA range:35-84 |
| 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Phospho-Chk2 (Thr68)抗体的3篇参考文献示例：
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1. **文献名称**：*Activation of the ATM Kinase by Ionizing Radiation and Phosphorylation of Chk2*
**作者**：Ahn, J., Urist, M., Prives, C.
**摘要**：该研究揭示了电离辐射诱导ATM激酶激活后，Chk2蛋白Thr68位点的磷酸化是其激活的关键步骤。作者通过Phospho-Chk2 (Thr68)抗体在Western blot中验证了DNA损伤后Chk2的磷酸化状态，并证实其依赖ATM激酶活性。
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2. **文献名称**：*DNA Damage Checkpoint Control in Cells Exposed to Ionizing Radiation*
**作者**：Matsuoka, S., Rotman, G., Ogawa, A., et al.
**摘要**：文章系统研究了DNA损伤检查点蛋白Chk2的激活机制，利用Phospho-Chk2 (Thr68)特异性抗体检测细胞辐射处理后Thr68位点的磷酸化，证明该修饰是Chk2寡聚化及下游信号传递的必要条件。
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3. **文献名称**：*Functional Analysis of hChk2 Mutants Reveals a Role for Phosphorylation in Activation*
**作者**：Schwarz, J.K., Lovly, C.M., Piwnica-Worms, H.
**摘要**：研究通过突变分析和Phospho-Chk2 (Thr68)抗体的免疫沉淀实验，证实Thr68磷酸化对Chk2激酶活性及细胞周期阻滞功能至关重要，并揭示了其与癌症相关突变的功能关联。
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(注：以上文献信息为示例，实际引用时请核对原文准确性。)
Phospho-Chk2 (Thr68) antibody is a specialized tool used to detect the activated form of checkpoint kinase 2 (Chk2), a key regulator of the DNA damage response (DDR) pathway. Chk2 is a serine/threonine kinase activated primarily in response to DNA double-strand breaks (DSBs) or replication stress. Its phosphorylation at Thr68. located in the N-terminal SQ/TQ cluster domain, serves as a critical marker of activation. This phosphorylation event is mediated by the upstream kinase ATM (ataxia-telangiectasia mutated), which is recruited to sites of DNA damage. Once phosphorylated, Chk2 undergoes a conformational change, leading to dimer dissociation, autophosphorylation, and full kinase activation. Activated Chk2 then phosphorylates downstream targets, such as p53. CDC25. and BRCA1. to enforce cell cycle arrest, DNA repair, or apoptosis, thereby maintaining genomic stability.
The Phospho-Chk2 (Thr68) antibody is widely used in research to study DDR mechanisms, cancer biology, and therapeutic responses. Its specificity allows scientists to assess Chk2 activation status in cells or tissues exposed to genotoxic agents (e.g., ionizing radiation, chemotherapeutics) or in models of genetic instability. Dysregulation of Chk2 signaling is linked to tumorigenesis, as mutations or altered expression can impair checkpoint control, promoting uncontrolled proliferation. This antibody is essential for elucidating how Chk2 contributes to cancer progression, treatment resistance, and as a potential biomarker for DDR-targeted therapies. Validation methods, including knockout controls or phosphatase treatment, are recommended to confirm signal specificity in experimental setups.
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