Human B7-H4 Alexa Fluor® 405-conjugated Antibody Summary
Phe29-Ala258
Accession # Q7Z7D3
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 VTCN1, B7x and B7S1, is a 50‑80 kDa glycosylated member of the BTN/MOG family of immunomodulatory protein (1, 2). Mature human B7-H4 consists of a 235 amino acid (aa) extracellular domain (ECD) with one Ig-like V-set domain and one Ig-like C2-set domain, a 21 aa transmembrane segment, and a 2 aa cytoplasmic tail (3-5). Within the ECD, human B7-H4 shares 90% aa sequence identity with mouse and rat B7-H4. It shares 22%-28% aa sequence identity with human B7-1, B7-2, B7-H1, B7-H2, B7-H3, and PD‑L2. Alternate splicing of human B7-H4 generates an additional isoform that lacks the first Ig-like domain. 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). Following binding to activated T cells, B7-H4 serves as a co‑inhibitor of the T cell response. This is accomplished by reverse signaling that can induce either cell cycle arrest, or apoptosis in B7-H4 expressing cells (3-5, 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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