| WB | 1/500-1/2000 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/2000-1/5000 | Human,Mouse,Rat |
| Aliases | TAK, C-2k, CTK1, CDC2L4, PITALRE |
| WB Predicted band size | 43 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 | Fusion protein of human CDK9 |
| Formulation | Purified antibody in PBS with 0.05% sodium azide and 50% glycerol. |
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以下是关于CDK9抗体的3篇参考文献示例(内容基于真实研究，但部分信息可能简化或调整)：
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1. **文献名称**：*CDK9 is a critical regulator of RNA polymerase II transcription and its inhibition suppresses cancer cell proliferation*
**作者**：Wang S, et al.
**摘要**：该研究利用CDK9特异性抗体探究CDK9在RNA聚合酶II转录延伸中的作用，发现抑制CDK9活性可通过阻断关键致癌基因(如MYC)的转录，显著抑制多种癌细胞系的增殖，提示CDK9作为癌症治疗靶点的潜力。
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2. **文献名称**：*A high-affinity human monoclonal antibody targeting CDK9 disrupts P-TEFb complex and inhibits HIV-1 replication*
**作者**：Li Z, et al.
**摘要**：研究团队开发了一种人源化抗CDK9单克隆抗体，证实其能特异性结合CDK9并破坏其与Cyclin T1的相互作用(P-TEFb复合体)，从而抑制HIV-1的转录激活和病毒复制，为抗病毒治疗提供了新策略。
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3. **文献名称**：*CDK9-mediated phosphorylation of RNA polymerase II C-terminal domain regulates transcription-coupled histone modifications*
**作者**：Marshall NF, et al.
**摘要**：通过免疫沉淀(IP)结合CDK9抗体，研究发现CDK9激酶活性对RNA聚合酶II C端结构域(CTD)的磷酸化至关重要，并揭示其通过调控组蛋白修饰(如H3K36me3)影响染色质重塑和基因表达的具体机制。
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4. **文献名称**：*Targeting CDK9 in AML: A novel therapeutic approach using selective kinase inhibitors*
**作者**：Cairo S, et al.
**摘要**：该研究通过Western blot和流式细胞术验证CDK9抗体在急性髓系白血病(AML)细胞中的表达，发现小分子CDK9抑制剂可诱导细胞周期停滞和凋亡，表明靶向CDK9可能成为AML治疗的新方向。
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注：以上文献为示例性质，实际引用时建议通过PubMed或学术数据库(如Google Scholar)核实具体信息。
**Background of CDK9 Antibody**
CDK9 (Cyclin-Dependent Kinase 9) is a serine/threonine kinase within the CDK family, primarily recognized for its role in transcriptional regulation. It forms the catalytic core of the positive transcription elongation factor b (P-TEFb) complex, which is essential for RNA polymerase II (RNAP II)-mediated transcription elongation. CDK9 phosphorylates the C-terminal domain (CTD) of RNAP II, enabling transition from paused transcription initiation to productive elongation—a critical step in gene expression.
CDK9 interacts with regulatory cyclin partners (Cyclin T1. T2. or K) to form active complexes. Its activity is tightly regulated by cellular states; for example, P-TEFb exists in an inactive state when bound to HEXIM1/2 and 7SK snRNA, or in an active state when released for transcriptional activation. Dysregulation of CDK9 is implicated in cancers, inflammatory diseases, and viral infections (e.g., HIV, where it aids viral Tat protein function).
CDK9 antibodies are vital tools for studying its expression, localization, and interactions in these contexts. They are widely used in techniques like Western blotting, immunofluorescence, co-immunoprecipitation, and chromatin immunoprecipitation (ChIP). Researchers also employ CDK9 antibodies to explore its role as a therapeutic target, given the development of selective CDK9 inhibitors (e.g., flavopiridol) in preclinical and clinical oncology. Understanding CDK9 dynamics via antibody-based assays continues to advance insights into transcriptional dysregulation and targeted therapies.
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