Human/Mouse B7-H4 Alexa Fluor® 750-conjugated Antibody Summary
Phe29-Pro258
Accession # Q7TSP5
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
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Preparation and Storage
Background: B7-H4
B7-H4, also known as B7x and B7S1, is a 50 ‑ 80 kDa glycosylated member of the B7 family of immune co‑stimulatory proteins (1, 2). Mature mouse B7-H4 consists of a 230 amino acid (aa) extracellular domain (ECD) with one Ig-like V-set domain and one Ig-like C2-set domain which is followed by a hydrophobic C-terminal region (3 - 5). 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 mouse B7-1, B7-2, B7-H1, B7-H2, B7‑H3, and PD-L2. B7-H4 is expressed on the surface of activated lymphocytes, macrophages, monocytes, dendritic cells, epithelial cells, and bone marrow-derived mesenchymal stem cells (4 - 8). Its binding to activated T cells dampens T cell responses and induces cell cycle arrest in the T cell (3 - 5). Reverse signaling can induce either cell cycle arrest or apoptosis in the B7-H4 expressing cell (9, 10). B7-H4 is up‑regulated in several carcinomas in correlation with tumor progression and metastasis (2, 7, 11, 12). A soluble form of B7-H4 is elevated in the serum of ovarian cancer, renal cell carcinoma, and rheumatoid arthritis patients, also in correlation with advanced disease status (13 - 15). Soluble B7-H4 functions as a decoy molecule that blocks the inhibitory influence of B7-H4 on immune activation (15). 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 (16).
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