Human Brain-Specific Angiogenesis Inhibitor 3 (BAI3) is a 177 kDa seven-span transmembrane (TM) protein, which is thought to be a member of the secretin receptor family. It is synthesized by neurons of the CNS and likely is a negative regulator of angiogenesis. BAI3 is 1498 amino acids in size. It contains three distinct regions: an N-terminal extracellular domain (ECD) (aa25-883), a 7-TM segment, and a C-terminal cytoplasmic region. The ECD contains four antiangiogenic TSP type 1 repeat (aa296-508), and one GSP domain (aa 816-867) that is likely used to cleave the ECD from the membrane-bound receptor. There is one altermate splice form that shows a deletion of aa 643-665. Over aa 25-880, human BAI3 shares 98% aa identity with mouse BAI3. BAI3 has been reported primarily in the brain, but is also localized to lung, testis, and pancreas. It might be involved in angiogenesis inhibition and suppression of glioblastoma.
BMP and activin membrane-bound inhibitor (BAMBI) is a transmembrane glycoprotein that is a pseudoreceptor of type 1 receptors. BAMBI structurally lacks intracellular serine/ threonine kinase domain but with an extracellular domain and a short cytoplasmic region that share sequence similarities with type 1 receptors, whose members have functions in signal transduction in various developing and pathological processes. BAMBI competes with the type 1 receptor, a receptor of the transforming growth factor-beta (TGF-beta), through functioning as negative regulators of TGF-beta by limiting the signaling range of the TGF-beta family during early embryogenesis. The expression of BAMBI can be induced by accumulated beta-catenin and BMP. The expression level of BAMBI was found aberrantly elevated in most colorectal and hepatocellular carcinomas relative to the corresponding non-cancerous tissues. It suggestes that beta-catenin and TGF-beta interfere growth arrest by inducing the expression of BAMBI, and this may contribute to colorectal and hepatocellular tumorigenesis.
B- and T-Lymphocyte Attenuator (BTLA) is a single-pass type I membrane protein containing 1 Ig-like V-type (immunoglobulin-like) domain. BTLA expression is induced during activation of T cells, and BTLA remains expressed on Th1 cells but not Th2 cells. Like PD1 and CTLA4, BTLA interacts with a B7 homolog, B7H4. However, unlike PD-1 and CTLA-4, BTLA displays T-Cell inhibition via interaction with tumor necrosis family receptors (TNF-R), not just the B7 family of cell surface receptors. BTLA is a lymphocyte inhibitory receptor that inhibits lymphocytes during immune response. BTLA also is a ligand for tumor necrosis factor (receptor) superfamily, member 14 (TNFRSF14), also known as herpes virus entry mediator (HVEM). BTLA-HVEM complexes negatively regulate T-cell immune responses.
Basigin/CD147 is a member of the immunoglobulin superfamily with homology to both the immunoglobulin V domain and MHC class II antigen beta-chain. This protein play important roles in variety of events including spermatogenesis, embryo implantation, neural network formation. CD147 induces the production and release of matrix metalloproteinases (MMP) in the surrounding mesenchymal cells and tumor cells, and thereby promotes invasion, metastasis, growth and survival of malignant cells. Furthermore, CD147 also serves as a receptor for extracellular cyclophilinthe and its association with integrins might be important in signal transduction. CD147 displays increased expression in many cancers, and it has been previously demonstrated to participate in cancer metastasis and progression.
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