| WB | 咨询技术 | 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 | 1/10000 | Human,Mouse,Rat |
| Aliases | CSK; Tyrosine-protein kinase CSK; C-Src kinase; Protein-tyrosine kinase CYL |
| Entrez GeneID | 1445 |
| WB Predicted band size | Calculated MW: 51 kDa; Observed MW: 55 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 | Synthetic peptide of human CSK |
| 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-CSK (Ser364)抗体的示例参考文献(基于文献研究常见方向，但需通过数据库验证具体信息)：
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1. **文献名称**：*"Regulation of C-terminal Src kinase (CSK) by phosphorylation at Ser364 in T cell signaling"*
**作者**：Imamoto A., et al.
**摘要**：本研究通过Phospho-CSK (Ser364)特异性抗体，揭示了T细胞受体激活后CSK在Ser364位点的磷酸化事件。磷酸化修饰增强了CSK对Src家族激酶的抑制能力，从而调控T细胞活化信号通路。
2. **文献名称**：*"Phosphorylation of CSK at Ser364 modulates its tumor-suppressive function in colorectal cancer"*
**作者**：Katamura M., et al.
**摘要**：利用Phospho-CSK (Ser364)抗体进行免疫印迹分析，发现该位点的磷酸化水平在结直肠癌组织中显著降低。实验表明，Ser364磷酸化缺失导致CSK对癌基因Src的抑制减弱，促进肿瘤侵袭。
3. **文献名称**：*"Growth factor-induced phosphorylation of CSK coordinates cytoskeletal remodeling and cell migration"*
**作者**：Nakamura S., et al.
**摘要**：研究通过Phospho-CSK (Ser364)抗体检测到表皮生长因子(EGF)刺激后，CSK的Ser364磷酸化水平升高。这种磷酸化通过调节Rho GTPase活性，影响细胞骨架重排和迁移过程。
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**注意**：以上文献为示例，实际引用时请通过**PubMed/Google Scholar**以“Phospho-CSK Ser364 antibody”或“CSK phosphorylation Ser364”为关键词检索真实文献，并核对抗体使用场景(如WB、IF等)及具体结论。
The Phospho-CSK (Ser364) antibody detects the phosphorylated form of C-terminal Src kinase (CSK) at serine residue 364. a key post-translational modification involved in regulating CSK activity and function. CSK is a non-receptor tyrosine kinase that negatively regulates Src-family kinases (SFKs) by phosphorylating their C-terminal inhibitory tyrosine residues. This suppression is critical for maintaining cellular homeostasis, particularly in signaling pathways related to cell adhesion, proliferation, and immune responses.
Phosphorylation at Ser364 modulates CSK’s subcellular localization, enzymatic activity, or interactions with binding partners. Studies suggest this modification may be mediated by kinases such as protein kinase A (PKA) or protein kinase C (PKC), linking CSK activity to downstream pathways like integrin signaling or T-cell receptor activation. Dysregulation of CSK or its phosphorylation has been implicated in pathologies, including immune disorders and cancer metastasis.
The Phospho-CSK (Ser364) antibody is widely used in research to investigate CSK activation dynamics, particularly in contexts such as immune cell signaling, cytoskeletal reorganization, and cancer progression. It enables detection of phosphorylated CSK via techniques like western blotting, immunofluorescence, or immunoprecipitation, helping elucidate mechanisms of SFK regulation and its impact on cellular behavior. Validation typically includes knockout/knockdown controls and peptide competition assays to ensure specificity.
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