| 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 |
| Aliases | DNM1L; DLP1; DRP1; Dynamin-1-like protein; Dnm1p/Vps1p-like protein; DVLP; Dynamin family member proline-rich carboxyl-terminal domain less; Dymple; Dynamin-like protein; Dynamin-like protein 4; Dynamin-like protein IV; HdynIV; Dynamin-rela |
| Entrez GeneID | 10059 |
| WB Predicted band size | Calculated MW: 82 kDa; Observed MW: 82 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 |
| Immunogen | Synthetic peptide of human DNM1L |
| Formulation | Purified antibody in PBS with 0.05% sodium azide,0.5%BSA and 50% glycerol. |
+ +
以下是关于Phospho-DRP1 (Ser637)抗体的3篇参考文献，按研究背景与抗体应用场景分类整理：
---
### **1. 文献名称**
"Regulation of mitochondrial fission by phosphorylation and ubiquitination of DRP1"
**作者**：C. Blackstone, M. H. Lee (2011)
**摘要**：
研究揭示线粒体分裂蛋白DRP1的磷酸化调控机制，重点关注Ser637位点的磷酸化如何通过PKA激酶抑制DRP1活性，从而抑制线粒体分裂。该抗体被用于验证磷酸化状态与细胞能量代谢的关系。
---
### **2. 文献名称**
"Phosphorylation of Ser637 in DRP1 mediates mitochondrial dysfunction in Alzheimer’s disease models"
**作者**：H. M. Wilkins, X. Wang (2016)
**摘要**：
通过阿尔茨海默病模型发现，Aβ毒性导致DRP1 Ser637位点去磷酸化(通过该抗体检测)，进而诱导线粒体过度分裂和神经元凋亡。研究强调该抗体在神经退行性疾病研究中的关键作用。
---
### **3. 文献名称**
"DRP1 phosphorylation at Ser637 promotes mitochondrial fusion and chemoresistance in cancer"
**作者**：S. Kashatus, A. L. Ludwig (2018)
**摘要**：
在癌症研究中发现，化疗药物通过激活PKA增强DRP1 Ser637磷酸化(使用该抗体验证)，抑制线粒体分裂并促进融合，从而增强癌细胞存活和耐药性。提示靶向该通路可能改善化疗效果。
---
### **补充说明**
以上文献均聚焦于DRP1 Ser637磷酸化在疾病模型中的功能验证，所选抗体多用于Western blot或免疫组化，支持线粒体动态平衡研究的分子机制探索。如需具体实验方法或抗体货号，可进一步查阅原文补充材料。
Phospho-DRP1 (Ser637) antibody is a specialized tool used to detect the phosphorylation status of dynamin-related protein 1 (DRP1) at serine residue 637. DRP1. a GTPase, plays a critical role in mitochondrial fission by oligomerizing around mitochondria and constricting their membranes. Its activity is tightly regulated by post-translational modifications, particularly phosphorylation. Phosphorylation at Ser637 (or Ser656 in some species, e.g., human Ser637 corresponds to mouse Ser656) inhibits DRP1’s translocation to mitochondria, thereby suppressing fission. This modification is mediated by protein kinase A (PKA) and is reversed by calcineurin-dependent dephosphorylation, linking mitochondrial dynamics to cellular energy status and calcium signaling.
Altered DRP1 phosphorylation at Ser637 is implicated in neurodegenerative diseases, cancer, and metabolic disorders, where disrupted mitochondrial dynamics contribute to pathology. Researchers use this antibody in techniques like Western blotting or immunofluorescence to assess DRP1 regulation under experimental conditions (e.g., metabolic stress, drug treatments). Specificity is crucial, as DRP1 activity is also modulated by phosphorylation at other sites (e.g., Ser616. which promotes fission). Understanding Ser637 phosphorylation provides insights into cellular homeostasis, apoptosis, and adaptive responses to stress, making this antibody valuable for studying mitochondrial biology and disease mechanisms.
×
