KMD Bioscience Co., Ltd.
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| Catalog Number | KMP2719 |
|---|---|
| Product Name | Human B7-H4 Protein, His Tag, Avi Tag |
| Product Description | The Human B7-H4 Protein(KMP2719) is produced in HEK293 Cells. The target gene encoding the human VTCN1 (NP_078902.2) (Phe29-Ala258) is expressed with a c-terminal polyhistidine tagged Avi tag at the C-terminus. The expressed protein is biotinylated in vivo by the Biotin-Protein ligase (BirA enzyme) which is co-expressed. |
| Molecular Name | B7-H4 |
| Alias | Human B7-H4 Protein, His Tag, Avi Tag, B7-H4 |
| Molecular Weight | 28.6 kDa |
| Species | Human |
| Size | 50ug, 100ug, 200ug |
| Host | HEK293 Cells |
| Purity | >95% as determined by SDS-PAGE |
| Endotoxin | <1.0 EU/ug determined by the LAL method |
| Buffer | PBS, pH7.4 |
| Purification | Affinity purification |
| Background | V-set domain-containing T-cell activation inhibitor 1, also known as B7X, B7H4, B7S1, and VTCN1, is a single-pass type-III membrane protein belonging to the B7 family of costimulatory proteins. These proteins are expressed on the surface of antigen-presenting cells and interact with ligands on T lymphocytes. They provide costimulatory signals that regulate T cell responses. A soluble form of B7H4 has also been detected. B7X / VTCN1 / B7H4 negatively regulates T-cell-mediated immune response by inhibiting T-cell activation, proliferation, cytokine production and development of cytotoxicity. When expressed on the cell surface of tumor macrophages, B7X / VTCN1 / B7H4 plays an important role, together with regulatory T-cells(Treg), in the suppression of tumor-associated antigen-specific T-cell immunity. B7X / VTCN1 / B7H4 is also involved in promoting epithelial cell transformation. This membrane protein can be up-regulated by IL6 / interleukin-6 and IL10 / interleukin-10 and inhibited by CSF2 / GM-CSF and IL4 / interleukin-4 on antigen-presenting cells. |
| Storage | Aliquot and store at -20℃ to -80℃. Avoid repeated freezing and thawing cycles. |
| Note | This product is for research use only. |
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