WB | 咨询技术 | Human,Mouse,Rat |
IF | 咨询技术 | Human,Mouse,Rat |
IHC | 1/50-1/200 | Human,Mouse,Rat |
ICC | 技术咨询 | Human,Mouse,Rat |
FCM | 咨询技术 | Human,Mouse,Rat |
Elisa | 1:20000-1:40000 | Human,Mouse,Rat |
Aliases | MYBL2, B-MYB, Myb-like protein 2, Myb-related protein B, BMYB |
Entrez GeneID | 4605; |
WB Predicted band size | 79kDa |
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 | A synthesized peptide derived from human B-Myb (Phospho-Thr494/497) |
Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于 B-Myb (Phospho-Thr494/497) 抗体的3篇参考文献示例(注:文献为虚构示例,仅作格式参考):
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1. **文献名称**: *Phosphorylation of B-Myb at Thr494/497 Regulates Its Transcriptional Activity During G2/M Phase*
**作者**: Johnson et al.
**摘要**: 本研究通过免疫印迹(Western blot)和免疫荧光技术,利用特异性B-Myb (Phospho-Thr494/497) 抗体,揭示了CDK1/cyclin B激酶介导的B-Myb磷酸化对其在G2/M期调控靶基因(如PLK1)的关键作用,并验证了该抗体的特异性。
2. **文献名称**: *PLK1-Dependent Phosphorylation of B-Myb Modulates DNA Damage Response*
**作者**: Chen et al.
**摘要**: 文章利用B-Myb (Phospho-Thr494/497) 抗体,证实了PLK1激酶在DNA损伤后磷酸化B-Myb的Thr494/497位点,促进其与DNA修复蛋白的相互作用,并通过流式细胞术分析显示磷酸化水平与细胞周期阻滞相关。
3. **文献名称**: *B-Myb Phosphorylation Status as a Prognostic Marker in Neuroblastoma*
**作者**: Müller et al.
**摘要**: 通过免疫组化(IHC)和Western blot分析临床样本,该研究使用B-Myb (Phospho-Thr494/497) 抗体证明,B-Myb的高磷酸化水平与神经母细胞瘤患者的不良预后显著相关,提示其作为潜在治疗靶点的价值。
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**注**:以上文献为示例,实际研究中需通过PubMed或专业数据库检索真实文献。
The B-Myb (Phospho-Thr494/497) antibody is designed to detect the phosphorylated form of the B-Myb protein at specific threonine residues (Thr494 and Thr497). B-Myb, encoded by the MYBL2 gene, is a transcription factor belonging to the Myb family, which plays critical roles in cell cycle progression, differentiation, and apoptosis. It is particularly active during the G1/S phase transition, regulating genes involved in DNA replication and mitotic control. Phosphorylation at Thr494 and Thr497. mediated by cyclin-dependent kinases (CDKs) such as CDK1/cyclin B during the G2/M phase, is essential for B-Myb’s transcriptional activation and stability. This post-translational modification enhances its ability to recruit coactivators and target genes necessary for mitotic entry and chromosome segregation.
The B-Myb (Phospho-Thr494/497) antibody is widely used in research to study cell cycle dynamics, DNA damage responses, and cancer biology, as B-Myb overexpression or dysregulation is linked to tumorigenesis. It enables specific detection of the activated form of B-Myb via techniques like Western blotting, immunofluorescence, and immunoprecipitation. Validation often includes testing in phosphorylation-deficient mutants or CDK inhibitor-treated cells to confirm specificity. Understanding B-Myb phosphorylation provides insights into mechanisms underlying cell proliferation and potential therapeutic targets in cancers with MYBL2 amplification or hyperactivity.
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