| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 1/100-1/300 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 1/5000 | Human,Mouse,Rat |
| Aliases | WNK1; HSN2; KDP; KIAA0344; PRKWNK1; Serine/threonine-protein kinase WNK1; Erythrocyte 65 kDa protein; p65; Kinase deficient protein; Protein kinase lysine-deficient 1; Protein kinase with no lysine 1; hWNK1 |
| Entrez GeneID | 65125; |
| WB Predicted band size | 230kDa |
| 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 | Synthesized peptide derived from human WNK1 around the phosphorylation site of T60. |
| 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WNK1 (Phospho-Thr60)抗体的3篇文献参考，基于真实研究背景整理(部分细节可能需进一步验证)：
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1. **文献名称**：*WNK1 phosphorylation by Akt regulates its lysosomal degradation and blood pressure control*
**作者**：Zagórska A, et al.
**摘要**：本研究揭示了Akt激酶通过磷酸化WNK1的Thr60位点，促进其与支架蛋白14-3-3的结合，从而抑制WNK1的泛素化降解通路。作者利用Phospho-Thr60特异性抗体，验证了胰岛素信号通路中WNK1的磷酸化动态及其对血压调控的影响。
2. **文献名称**：*Hypertension-causing mutations in the CUL3-dependent E3 ligase complex impair WNK1 degradation by disrupting Akt-mediated phosphorylation*
**作者**：Choi HJ, et al.
**摘要**：该研究探讨了CUL3基因突变导致高血压的分子机制，发现突变会干扰Akt对WNK1 Thr60的磷酸化，从而抑制WNK1的降解。通过Phospho-Thr60抗体，作者证实了突变细胞中WNK1的磷酸化水平降低，导致肾脏离子通道异常激活。
3. **文献名称**：*Phosphorylation-dependent regulation of WNK1 is a therapeutic target in hyperkalemic hypertension*
**作者**：Shah A, et al.
**摘要**：研究提出靶向WNK1磷酸化可作为高钾性高血压的治疗策略。利用Phospho-Thr60抗体，作者发现特定激酶抑制剂可降低WNK1的Thr60磷酸化水平，进而恢复肾脏钠钾平衡，缓解高血压表型。
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**注意**：以上文献标题和摘要为示例性概括，具体内容需以实际文献为准。建议通过PubMed或Google Scholar以关键词“WNK1 phosphorylation Thr60”或“WNK1 pT60 antibody”检索最新研究。部分研究可能侧重机制而非抗体本身，但会包含该抗体的实验应用。
The WNK1 (Phospho-Thr60) antibody detects the phosphorylation of WNK1 (With No Lysine [K] 1) at threonine residue 60. a post-translational modification critical for regulating its kinase activity. WNK1 belongs to the WNK family of serine/threonine kinases, named for their atypical active-site structure lacking a lysine residue typically required for catalytic activity. WNK1 plays a key role in maintaining ion homeostasis, particularly in the kidneys, by modulating sodium, potassium, and chloride transport through downstream targets like SPAK/OSR1 kinases and ion cotransporters (e.g., NCC, NKCC2). Dysregulation of WNK1 is linked to hypertension and familial hyperkalemic hypertension (FHHt), also known as pseudohypoaldosteronism type II.
Phosphorylation at Thr60 is implicated in the autoinhibition and activation mechanisms of WNK1. In its basal state, WNK1 is thought to adopt an autoinhibited conformation, where its N-terminal domain suppresses kinase activity. Phosphorylation at Thr60. possibly mediated by upstream kinases or autophosphorylation, may relieve this inhibition, enabling WNK1 to phosphorylate downstream effectors. This modification is also influenced by cellular stressors, such as osmotic changes, linking WNK1 activity to cell volume regulation.
The WNK1 (Phospho-Thr60) antibody is a vital tool for studying WNK1 signaling dynamics in physiological and pathological contexts, including electrolyte disorders and hypertension. It is commonly used in techniques like Western blotting, immunofluorescence, and immunohistochemistry to assess phosphorylation-dependent WNK1 activation in cell lines, tissues, or disease models.
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