- 全部删除
- 您的购物车当前为空
ADAM17 is a member of the ADAM protein family of disintegrins and metalloproteases. ADAM17 is ubiquitously expressed in the human colon, with increased activity in the colonic mucosa of patients with ulcerative colitis, a main form of inflammatory bowel disease. The expression of ADAM17 may be inhibited by ethanol. It is involved in the processing of tumor necrosis factor alpha (TNF-α) at the surface of the cell, and from within the intracellular membranes of the trans-Golgi network. ADAM17 also plays a role in the release of a diverse variety of membrane-anchored cytokines, cell adhesion molecules, receptors, ligands, and enzymes. ADAM17 may play a prominent role in the Notch signaling pathway, during the proteolytic release of the Notch intracellular domain (from the Notch1 receptor) that occurs following ligand binding.
规格 | 价格 | 库存 | 数量 |
---|---|---|---|
20 μg | ¥ 3,820 | 5日内发货 |
生物活性 | Measured by its ability to cleave a fluorogenic peptide substrate Mca-PLAQAV-Dpa-RSSSR-NH2 . The specific activity is >250 pmol/min/µg. |
产品描述 | ADAM17 is a member of the ADAM protein family of disintegrins and metalloproteases. ADAM17 is ubiquitously expressed in the human colon, with increased activity in the colonic mucosa of patients with ulcerative colitis, a main form of inflammatory bowel disease. The expression of ADAM17 may be inhibited by ethanol. It is involved in the processing of tumor necrosis factor alpha (TNF-α) at the surface of the cell, and from within the intracellular membranes of the trans-Golgi network. ADAM17 also plays a role in the release of a diverse variety of membrane-anchored cytokines, cell adhesion molecules, receptors, ligands, and enzymes. ADAM17 may play a prominent role in the Notch signaling pathway, during the proteolytic release of the Notch intracellular domain (from the Notch1 receptor) that occurs following ligand binding. |
种属 | Rat |
表达系统 | HEK293 Cells |
标签 | C-His |
蛋白编号 | Q9Z1K9 |
别名 | ADAM metallopeptidase domain 17 |
蛋白构建 | A DNA sequence encoding the rat ADAM17 (Q9Z1K9) (Met1-Asp563) was expressed with a polyhistidine tag at the C-terminus. Predicted N terminal: Pro 18 |
蛋白纯度 | > 95 % as determined by SDS-PAGE |
分子量 | 63 kDa (predicted); 57 and 20 kDa (reducing condition, due to glycosylation) |
内毒素 | < 1.0 EU/μg of the protein as determined by the LAL method. |
缓冲液 | Lyophilized from a solution filtered through a 0.22 μm filter, containing PBS, pH 7.4. Typically, a mixture containing 5% to 8% trehalose, mannitol, and 0.01% Tween 80 is incorporated as a protective agent before lyophilization. |
复溶方法 | A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information. |
存储 | It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots. |
运输方式 | In general, Lyophilized powders are shipping with blue ice. |
研究背景 | ADAM17 is a member of the ADAM protein family of disintegrins and metalloproteases. ADAM17 is ubiquitously expressed in the human colon, with increased activity in the colonic mucosa of patients with ulcerative colitis, a main form of inflammatory bowel disease. The expression of ADAM17 may be inhibited by ethanol. It is involved in the processing of tumor necrosis factor alpha (TNF-α) at the surface of the cell, and from within the intracellular membranes of the trans-Golgi network. ADAM17 also plays a role in the release of a diverse variety of membrane-anchored cytokines, cell adhesion molecules, receptors, ligands, and enzymes. ADAM17 may play a prominent role in the Notch signaling pathway, during the proteolytic release of the Notch intracellular domain (from the Notch1 receptor) that occurs following ligand binding. |
版权所有©2015-2024 TargetMol Chemicals Inc.保留所有权利.