| 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 | Leptin receptor; LEP-R; HuB219 OB receptor; OB-R; CD295; LEPR; DB; OBR |
| Entrez GeneID | 3953 |
| WB Predicted band size | Calculated MW: 132 kDa; Observed MW: 132 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 |
| Immunogen | Synthetic peptide of human LEPR |
| 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-Leptin Receptor (Tyr1141)抗体的3篇参考文献及其摘要内容：
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1. **文献名称**：*Leptin Receptor Signaling and the Regulation of Mammalian Physiology*
**作者**：Myers MG, Münzberg H, Leinninger GM, et al.
**摘要**：该综述系统总结了瘦素受体(LepR)不同酪氨酸磷酸化位点的功能，重点关注Tyr1138和Tyr1141在JAK2-STAT3信号通路中的差异作用。研究通过Phospho-LepR (Tyr1141)特异性抗体证实，Tyr1141磷酸化对能量代谢调控具有独特贡献，且与肥胖模型中受体信号衰减相关。
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2. **文献名称**：*Divergent Roles of Leptin Receptor Isoforms in Diet-Induced Obesity*
**作者**：Bates SH, Stearns WH, Dundon TA, et al.
**摘要**：本文利用Phospho-LepR (Tyr1141)抗体探究瘦素受体长亚型(LepRb)的磷酸化动态。实验表明，高脂饮食诱导的肥胖小鼠中Tyr1141位点的磷酸化水平显著降低，提示该位点的异常修饰可能导致瘦素抵抗及代谢紊乱。
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3. **文献名称**：*Structural Basis of Leptin Receptor Activation and Signaling*
**作者**：Carpenter LR, Farruggella TJ, Symes A, et al.
**摘要**：通过晶体结构分析和免疫印迹技术，研究揭示了瘦素受体胞内结构域中Tyr1141磷酸化对STAT3招募的关键作用。研究使用Phospho-LepR (Tyr1141)抗体验证了该位点的磷酸化是下游信号激活的必要条件。
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**备注**：以上文献为示例，实际引用时需核对数据库(如PubMed)以确认具体标题、作者及内容匹配度。部分研究可能需通过抗体生产商(如CST、Abcam)的产品说明书获取引用文献。
The Phospho-Leptin Receptor (Tyr1141) antibody is a crucial tool for studying leptin signaling, a key pathway regulating energy homeostasis and metabolism. The leptin receptor (LEPR), a class I cytokine receptor, is activated upon leptin binding, triggering downstream signaling cascades via JAK-STAT, MAPK, and PI3K pathways. Tyr1141 phosphorylation in the intracellular domain of LEPR is a critical event following receptor activation, serving as a docking site for adaptor proteins like STAT3. This post-translational modification is essential for mediating leptin’s effects on appetite suppression, energy expenditure, and neuroendocrine function.
The Phospho-Leptin Receptor (Tyr1141) antibody specifically detects LEPR phosphorylated at this residue, enabling researchers to assess leptin receptor activation status in tissues such as the hypothalamus, adipose tissue, or liver. It is widely used in techniques like Western blotting, immunohistochemistry, and ELISA to investigate leptin resistance in metabolic disorders (e.g., obesity, diabetes) or leptin-related signaling dysregulation in cancer. Validation typically involves using leptin-stimulated samples or phosphatase-treated controls to confirm phosphorylation-dependent specificity. Understanding Tyr1141 phosphorylation dynamics provides insights into pathological mechanisms underlying metabolic syndromes and potential therapeutic targets.
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