| WB | 1/500-1/1000 | 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 | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | NS; NETS; LEKTI; LETKI; VAKTI |
| Entrez GeneID | 11005 |
| WB Predicted band size | Calculated MW: 121 kDa; Observed MW: 121 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 | A synthetic peptide of human SPINK5 |
| Formulation | Purified antibody in TBS with 0.05% sodium azide,0.05%BSA and 50% glycerol. |
+ +
以下是3篇与SPINK5抗体相关的代表性文献摘要：
1. **文献名称**：*Mutations in SPINK5. encoding a serine protease inhibitor, cause Netherton syndrome*
**作者**：Chavanas S. et al.
**摘要**：该研究首次揭示了SPINK5基因突变导致Netherton综合征(一种严重的皮肤屏障缺陷疾病)，并指出SPINK5编码的LEKTI蛋白通过抑制蛋白酶活性维持表皮稳态，为后续开发针对LEKTI的抗体检测奠定基础。
2. **文献名称**：*LEKTI proteolytic processing in human primary keratinocytes, tissue distribution and defective expression in Netherton syndrome*
**作者**：Descargues P. et al.
**摘要**：通过使用特异性抗体分析LEKTI蛋白在皮肤中的表达，发现Netherton综合征患者因SPINK5突变导致LEKTI完全缺失，证明抗体检测可作为该病的诊断工具。
3. **文献名称**：*Elastase 2 is expressed in human and mouse epidermis and impairs skin barrier function in Netherton syndrome through filaggrin and lipid misprocessing*
**作者**：Bitoun E. et al.
**摘要**：研究利用SPINK5抗体发现LEKTI缺失会增强丝氨酸蛋白酶活性，导致角质层结构异常，强调了SPINK5/LEKTI在皮肤屏障中的关键作用。
4. **文献名称**：*SPINK5 is associated with early-onset and IgE-mediated atopic dermatitis in the Japanese population*
**作者**：Takayama K. et al.
**摘要**：通过检测患者SPINK5表达水平，发现其与IgE介导的特应性皮炎相关，提示针对SPINK5的抗体研究可能为过敏性疾病提供生物标志物。
这些研究均涉及SPINK5基因编码的蛋白功能及其抗体在疾病机制探索或诊断中的应用。
The SPINK5 gene encodes LEKTI (lympho-epithelial Kazal-type-related inhibitor), a serine protease inhibitor critical for maintaining epidermal integrity. Primarily expressed in skin and mucosal epithelia, LEKTI regulates proteolytic enzymes like kallikreins, preventing excessive degradation of proteins involved in keratinocyte cohesion and barrier function. Mutations in SPINK5 cause Netherton syndrome, a severe autosomal recessive disorder characterized by congenital ichthyosis, hair shaft defects, and atopic manifestations due to uncontrolled protease activity and barrier disruption.
SPINK5 antibodies are essential tools for studying this protein's expression, localization, and functional deficiencies. In research, they help visualize LEKTI distribution in epidermal layers via immunohistochemistry and quantify its levels in biological samples using ELISA or Western blot. Clinically, these antibodies aid in diagnosing Netherton syndrome by detecting absent or truncated LEKTI in skin biopsies. Recent studies also explore SPINK5/LEKTI's role in inflammatory skin diseases (e.g., atopic dermatitis) and its potential as a therapeutic target. However, antibody specificity remains challenging due to LEKTI's complex splicing variants and structural homology with other Kazal-type inhibitors. Ongoing work focuses on optimizing antibodies for functional studies and translational applications in dermatology.
×
