金山科研平台，产品价格货期咨询微信：jinshanbio Source:Mouse myeloma cell line, NS0-derived, Phe29-Ala258, with a C-terminal 10-His tag Accession #:NP_078902 N-terminal Sequence Analysis:Phe29 Purity:>95%, by SDS-PAGE under reducing conditions and visualized by silver stain. Endotoxin Level: Predicted Molecular Mass:26.7 kDa SDS-PAGE:45-60 kDa, reducing conditions Activity:Measured by its ability to inhibit anti-CD3 antibody induced IL-2 secretion in human T lymphocytes.The ED₅₀ for this effect is typically 0.5 -2.5 µg/mL. Formulation:Lyophilized from a 0.2 µm filtered solution in PBS.See Certificate of Analysis for details. Molecule Information: B7-H4 Long Name: B7 Homolog 4 Aliases: B7S1; B7x; Vtcn1 Entrez Gene IDs: 79679 (Human); 242122 (Mouse) Background: B7-H4

B7-H4, also known as B7x and B7S1, is a member of the B7 family of immune costimulatory proteins. Mature B7-H4 is a 50 kDa - 80 kDa glycosylated molecule with a 28 kDa protein core. Partial sensitivity to cleavage by PI-PLC suggests a possible GPI linkage of mouse B7-H4 to the cell membrane. The 230 aa extracellular region of B7-H4 contains one Ig-like V-set domain and one Ig-like C2-set domain which is followed by a hydrophobic C-terminal region. Within the ECD, mouse B7-H4 shares 90% and 99% aa sequence identity with human and rat B7-H4, respectively. It shares 21% - 29% aa sequence identity with B7-1, B7-2, B7-H1, B7-H2, B7-H3, and PD-L2.

B7-H4 expression is induced on mitogen- or LPS-activated B cells, T cells, dendritic cells, monocytes, and macrophages and blocked by GM-CSF or IL-4. It is also expressed on various normal epithelia and upregulated in several carcinomas and renal tubule epithelial cell lesions. B7-H4 is expressed on the surface of macrophages but intracellularly in ovarian and breast cancer cells. It is found in the serum and ascites fluid of cancer patients. B7-H4 binds an unidentified ligand on activated T cells which is distinct from BTLA, CD28, CTLA4, ICOS, and PD-1. Exposure to B7-H4 inhibits antigen-dependent induction of T cell proliferation and activation. Alternatively, B7-H4 expressing renal tubular epithelial cells promote T cell activation. Regulatory T cells, IL-6, and IL-10 induce B7-H4 expression on antigen presenting cells which fosters tumor growth by dampening the anti-tumor immune response. B7-H4 also promotes the malignant transformation of epithelial cells by protecting them from apoptosis. Despite evidence for the involvement of B7-H4 in immune regulation, mice deficient in its expression do not show significant immune deficiencies, suggesting compensation by other molecules in vivo.