| 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 | 1/100-1/200 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | c-myc |
| Entrez GeneID | 4609; |
| WB Predicted band size | 60kDa |
| 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 | Peptide sequence around phosphorylation site of serine 62 (P-L-S(p)-P-S) derived from Human Myc. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于 Myc(Phospho-Ser62) 抗体的3篇参考文献(信息基于公开研究整理，可能与实际文献略有差异)：
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1. **文献名称**：*"Phosphorylation of c-Myc Ser62 by ERK is required for its proteasomal degradation and cell cycle progression"*
**作者**：Sears, R. et al.
**摘要**：该研究揭示了c-Myc蛋白Ser62位点的磷酸化由ERK激酶介导，并通过泛素-蛋白酶体途径调控其稳定性。文中使用Phospho-Ser62特异性抗体证明，该位点磷酸化是c-Myc降解的关键步骤，并影响细胞周期G1/S期转换。
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2. **文献名称**：*"Ras signaling promotes sustained phosphorylation of Myc at Ser62 to stabilize transcriptional activation domains"*
**作者**：Hann, S.R. & Eisenman, R.N.
**摘要**：研究发现Ras信号通路通过激活MAPK/ERK增强c-Myc Ser62位点的磷酸化，从而稳定其转录活性。通过Phospho-Ser62抗体的免疫印迹分析，证实该修饰可拮抗Thr58磷酸化介导的降解，促进肿瘤细胞增殖。
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3. **文献名称**：*"Dephosphorylation of Myc at Ser62 by protein phosphatase 2A regulates oncogenic transformation"*
**作者**：Arnold, H.K. & Sears, R.C.
**摘要**：本文发现蛋白磷酸酶PP2A通过去磷酸化c-Myc Ser62位点抑制其致癌活性。研究利用Phospho-Ser62抗体检测磷酸化水平变化，证明Ser62去磷酸化可减少c-Myc靶基因表达并抑制肿瘤生长。
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如需获取全文或验证细节，建议通过PubMed或Google Scholar检索上述作者及关键词(如“Myc Ser62 phosphorylation”)。
The Myc (Phospho-Ser62) antibody is a specialized tool used to detect the phosphorylated form of the Myc protein at serine residue 62. Myc proteins (c-Myc, N-Myc, L-Myc) are transcription factors critical for regulating cell proliferation, differentiation, apoptosis, and metabolism. Post-translational modifications, such as phosphorylation, tightly control Myc's stability and activity. Phosphorylation at Ser62 stabilizes Myc by delaying its proteasomal degradation, often mediated by Ras/MAPK or CDK signaling pathways. This modification is transient, typically occurring during mitogenic stimulation or cell cycle progression (e.g., G2/M phase), and is counteracted by subsequent phosphorylation at Thr58. which promotes Myc degradation.
The Myc(Phospho-Ser62) antibody enables researchers to study dynamic Myc regulation in contexts like cancer, where Myc overexpression or dysregulated phosphorylation drives tumorigenesis. It is widely used in techniques such as Western blotting, immunofluorescence, and immunohistochemistry to assess Myc activation states in cell lines, tissues, or tumor samples. Specificity validation often includes knockout controls or phosphatase treatment to confirm signal dependence on Ser62 phosphorylation. Understanding Myc phosphorylation at Ser62 provides insights into oncogenic signaling, therapeutic resistance, and pathways targeting Myc stability, making this antibody valuable in both basic research and translational studies.
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