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产品简介
| Known as | Tumor necrosis factor receptor superfamily member 3;Lymphotoxin-beta receptor;Ltbr;Tnfcr;Tnfrsf3 |
| Derived from | Human Cells |
| Purity | Greater than 95% as determined by reducing SDS-PAGE. |
| Formulation | Lyophilized from a 0.2 μm filtered solution of PBS, pH7.4. |
| Storage | Lyophilized protein should be stored at < -20°C, though stable at room temperature for 3 weeks.Reconstituted protein solution can be stored at 4-7°C for 2-7 days.Aliquots of reconstituted samples are stable at < -20°C for 3 months. |
| Reconstitution | Always centrifuge tubes before opening. Do not mix by vortex or pipetting.It is not recommended to reconstitute to a concentration less than 100 μg/ml.Dissolve the lyophilized protein in distilled water.Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
| Endotoxin | Less than 0.1 ng/μg (1 EU/μg) as determined by LAL test. |
| Background | It is a single-pass type I membrane protein and contains 4 TNFR-Cys repeats. The protein is a member of the tumor necrosis factor (TNF) family of receptors. It is expressed on the surface of most cell types, including cells of epithelial and myeloid lineages, but not on T and B lymphocytes. The protein is the receptor for the heterotrimeric lymphotoxin containing LTA and LTB, and for TNFS14/LIGHT. It promotes apoptosis via TRAF3 and TRAF5 and may play a role in the development of lymphoid organs. The encoded protein and its ligand play a role in the development and organization of lymphoid tissue and transformed cells. Activation of the encoded protein can trigger apoptosis. Not only does the TNFRSF3 help trigger apoptosis, it can lead to the release of the cytokine interleukin 8. Overexpression of TNFRSF3 in Human Cells cells increases IL-8 promoter activity and leads to IL-8 release. TNFRSF3 is also essential for development and organization of the secondary lymphoid organs and chemokine release. |
| 规格 | 10ug50ug500ug1mg |
注意：
1.本产品仅供科研使用。请勿用于医药、临床诊断或治疗，食品及化妆品等用途。请勿存放于普通住宅区。
2.为了您的安全和健康，请穿好实验服并佩戴一次性手套和口罩操作。
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