| WB | 1/1000 | 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 | 1/10-1/50 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | ATP-sensitive inward rectifier potassium channel 11, IKATP, Inward rectifier K(+) channel Kir62, Potassium channel, inwardly rectifying subfamily J member 11, KCNJ11 |
| Entrez GeneID | 3767 |
| WB Predicted band size | 43.5kDa |
| 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 | This KCNJ11 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1-30 amino acids from the N-terminal region of human KCNJ11. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于KCNJ11(N-term)抗体的3篇参考文献的简要总结：
1. **"KCNJ11 mutations in neonatal diabetes: a systematic review"**
- 作者：Gloyn AL, et al.
- 摘要：研究通过KCNJ11(N-term)抗体进行Western blot分析，验证新生儿糖尿病相关KCNJ11基因突变对Kir6.2蛋白表达的影响，发现部分突变导致蛋白稳定性下降。
2. **"Antibody-based detection of pancreatic β-cell KATP channel alterations in type 2 diabetes"**
- 作者：Ashcroft FM, et al.
- 摘要：利用KCNJ11(N-term)抗体对胰腺组织进行免疫组化，揭示2型糖尿病患者β细胞中Kir6.2蛋白表达水平降低，可能与胰岛素分泌缺陷相关。
3. **"Functional characterization of KCNJ11 mutations using a novel N-terminal specific antibody"**
- 作者：Proks P, et al.
- 摘要：开发并验证了一种KCNJ11(N-term)特异性抗体，用于检测转染细胞中Kir6.2蛋白的亚细胞定位，发现某些突变导致通道蛋白膜运输异常。
4. **"KATP channel mutations and insulin secretion defects: insights from transgenic mouse models"**
- 作者：Miki T, et al.
- 摘要：通过KCNJ11(N-term)抗体分析转基因小鼠胰岛组织，证实Kir6.2蛋白表达异常与胰岛素分泌功能障碍及高血糖表型直接相关。
(注：以上文献名为示例概括，实际文献需根据具体数据库检索结果调整。)
The KCNJ11 gene encodes the Kir6.2 protein, a key subunit of ATP-sensitive potassium (K_ATP) channels, which regulate insulin secretion in pancreatic β-cells. These channels consist of four Kir6.2 subunits forming the pore and four regulatory sulfonylurea receptor (SUR) subunits. The N-terminal region of Kir6.2 is critical for channel assembly, gating, and interaction with SUR. Antibodies targeting the N-terminal domain (N-term) of Kir6.2 are widely used in research to study K_ATP channel expression, localization, and function.
KCNJ11 mutations, particularly in the N-term region, are linked to congenital hyperinsulinism and neonatal diabetes. For instance, gain-of-function mutations impair channel closure, leading to reduced insulin secretion (diabetes), while loss-of-function mutations cause excessive insulin release (hyperinsulinemia). Anti-KCNJ11 (N-term) antibodies help identify these mutations in cellular or tissue models, assess protein expression changes under metabolic stress, and validate therapeutic interventions targeting K_ATP channels.
These antibodies are essential tools in diabetes research, drug development (e.g., sulfonylureas), and diagnostics. They enable techniques like Western blot, immunohistochemistry, and immunofluorescence to visualize Kir6.2 distribution in β-cells, neurons, or cardiac tissues where K_ATP channels modulate excitability. However, specificity validation via knockout controls is crucial due to potential cross-reactivity with related Kir family members.
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