Butyrophilin Subfamily 3 Member A1 (BTN3A1/CD277) is a type I transmembrane glycoprotein member of the Ig superfamily. It is expressed on a wide variety of immune cells. Similar to BTN3A2 and BTN3A3, BTN3A1 is composed of an extracellular N-terminal IgV and a membraneproximal IgC domain followed by a transmembrane domain and a cytoplasmic tail. These Ig domains are also found in B7 family costimulatory molecules, suggesting structural and functional similarities between the two protein families. BTN3A1 acts as a critical protein for the activation of Vγ9Vδ2 T cells following detection of distressed cells. The anti-tumor responses of Vγ9Vδ2 T cells may be enhanced with agonistic anti-BTNA3 antibodies.
Tumor necrosis factor receptor superfamily; member 19 (TNFRSF19); also known as TAJ-alpha or TROY; is a member of the TNF-receptor superfamily. TNFRSF19/TROY expression is detected in the pulmonary epithelium and the ductal epithelium of the prostate and parotid glands. TNFRSF19/TROY expression is detected in some adenocarcinoma cell lines that arise from this tissue. It has been shown to interact with TRAF family members; and to activate JNK signaling pathway when overexpressed in cells. TNFRSF19/TROY is capable of inducing apoptosis by a caspase-independent mechanism; and it is thought to play an essential role in embryonic development. TNFRSF19/TROY was negatively regulated by adipogenic transcription factor CCAAT/enhancer-binding proteins (C/EBP). TNFRSF19 signals activation of the Jnk pathway and induces cell death. Overexpression of TNFRSF19 also signals NFB activation; comparable and similar to that by p75NGFR. TNFRSF19/TROY is capable of activating key signaling pathways of the TNF receptor family; and its predominant expression patterns suggest that it plays a role in the growth and regulation of epithelial tissues.
Human BTN3A3, also known as butyrophilin subfamily 3 member A3 and BTF3, is a Single-pass type I membrane protein which belongs to the immunoglobulin superfamily and BTN/MOG family. The butyrophilin (BTN) genes are a group of major histocompatibility complex (MHC)-associated genes that encode type I membrane proteins with 2 extracellular immunoglobulin domains and an intracellular B30.2 (PRYSPRY) domain. It can be detected in peripheral blood mononuclear cells, T-cells l, spleen and lymphocytes. BTN3A3 plays a role in T-cell responses in the adaptive immune response.
Butyrophilin-Like Protein 9 (BTNL9) is single-pass type I membrane protein member of the BTN/MOG family that belongs to the immunoglobulin superfamily. BTNL9 consists of two domains: one B30.2/SPRY domain and one Ig-like V-type (immunoglobulin-like) domain. Human BTNL9 mRNA has been identified in adipose, lung, thymus, spleen, colon, and cardiac tissues, but its highest levels of expression were found in B cells. BTNL9 expression has also been found to be down-regulated in colon cancer tumors.
β-Ureidopropionase is a cytoplasmic protein which belongs to the CN hydrolase family of BUP subfamily. β-Ureidopropionase binds one zinc ion per subunit, catalyzes the last step in the pyrimidine degradation pathway. β-Ureidopropionase can convert N-carbamyl-beta-aminoisobutyric acid and N-carbamyl-beta-alanine to beta-aminoisobutyric acid and beta-alanine, ammonia and carbon dioxide, respectively. The pyrimidine bases uracil and thymine are degraded via the consecutive action of dihydropyrimidine dehydrogenase (DHPDH), dihydropyrimidinase (DHP) and beta-ureidopropionase (UP) to beta-alanine and beta aminoisobutyric acid, respectively. Defects in β-Ureidopropionase are the cause of β-Ureidopropionase deficiency that is characterized by muscular hypotonia, dystonic movements, scoliosis, microcephaly and severe developmental delay.
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