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Rabbit Polyclonal Bim(Phospho-Thr56/116) Antibody

  • 中文名: Bim (Phospho-Thr56/116)抗体
  • 别    名: BCL2L11, BIM-alpha6, BIM-beta7, Bcl-2-like protein 11, BIM-beta6, BimL, BimS, Bcl-2 interacting protein Bim, BimEL, BAM, Bcl2-L-11, BIM, BOD
货号: IPDX41077
Price: ¥1280
数量:
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验证与应用

应用及物种
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 咨询技术 Human,Mouse,Rat

产品详情

AliasesBCL2L11, BIM-alpha6, BIM-beta7, Bcl-2-like protein 11, BIM-beta6, BimL, BimS, Bcl-2 interacting protein Bim, BimEL, BAM, Bcl2-L-11, BIM, BOD
Entrez GeneID10018;
WB Predicted band size25kDa,22kDa
Host/IsotypeRabbit IgG
Antibody TypePrimary antibody
StorageStore at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles.
Species ReactivityHuman,Mouse,Rat
ImmunogenA synthesized peptide derived from human Bim (Phospho-Thr56/116)
FormulationPurified antibody in PBS with 0.05% sodium azide.

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参考文献

以下是关于Bim (Phospho-Thr56/116)抗体的3篇参考文献示例:

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1. **文献名称**:*ERK-mediated phosphorylation of Bim inhibits apoptosis via regulation of 14-3-3 binding*

**作者**:Ley, R., et al.

**摘要**:该研究利用Phospho-Thr56/116特异性抗体,证明ERK激酶通过磷酸化Bim蛋白的Thr56/Thr116位点,促进其与14-3-3蛋白的结合,从而抑制Bim的促凋亡功能。

2. **文献名称**:*Proapoptotic Bcl-2 family member Bim is regulated by JNK phosphorylation in neuronal cells*

**作者**:Lu, Z., et al.

**摘要**:通过Phospho-Thr56/116抗体检测,作者发现JNK信号通路在神经元细胞中磷酸化Bim的Thr56/116位点,增强Bim稳定性并促进细胞凋亡,揭示了Bim在应激反应中的调控机制。

3. **文献名称**:*Phosphorylation of Bim-EL by Erk1/2 on serine 69 promotes its degradation via the proteasome*

**作者**:Akiyama, T., et al.

**摘要**:研究使用磷酸化特异性抗体验证了Bim-EL亚型中Thr56/116位点的磷酸化可被ERK1/2调控,导致其泛素化降解,并降低细胞凋亡敏感性。

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注:以上文献为示例,实际引用需根据具体研究内容核实(部分内容可能涉及Bim其他磷酸化位点的研究)。

背景信息

The Bim (Phospho-Thr56/116) antibody is designed to detect Bim protein when phosphorylated at threonine residues 56 and 116. key post-translational modifications regulating its pro-apoptotic activity. Bim (Bcl-2-interacting mediator of cell death), a BH3-only member of the Bcl-2 family, promotes apoptosis by neutralizing anti-apoptotic Bcl-2 proteins or directly activating Bax/Bak. Its activity is tightly controlled via phosphorylation-dependent degradation. Phosphorylation at Thr56 (by ERK/MAPK) and Thr116 (by JNK or other stress-activated kinases) triggers ubiquitination and proteasomal degradation, reducing Bim's apoptotic capacity. Conversely, dephosphorylation stabilizes Bim, enhancing cell death under stress. This antibody is widely used to study apoptotic signaling in cancer, neurodegenerative diseases, and immune regulation, particularly in contexts where survival pathways (e.g., RAS/ERK) are hyperactive. It helps assess Bim inactivation mechanisms in therapy resistance or evaluate stress-induced apoptosis in experimental models. Validation often involves treatments with kinase inhibitors (e.g., MEK inhibitors) or apoptotic stimuli to observe phosphorylation changes. Proper controls (e.g., phosphorylation-deficient mutants) are essential to confirm specificity. Understanding Bim phosphorylation dynamics provides insights into cellular fate decisions and therapeutic strategies targeting Bcl-2 family interactions.

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