|Other Names||Tumor necrosis factor receptor superfamily member 25, Apo-3, Apoptosis-inducing receptor AIR, Apoptosis-mediating receptor DR3, Apoptosis-mediating receptor TRAMP, Death receptor 3, Lymphocyte-associated receptor of death, LARD, Protein WSL, Protein WSL-1, TNFRSF25, APO3, DDR3, DR3, TNFRSF12, WSL, WSL1|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Synonyms||APO3, DDR3, DR3, TNFRSF12, WSL, WSL1|
|Function||Receptor for TNFSF12/APO3L/TWEAK. Interacts directly with the adapter TRADD. Mediates activation of NF-kappa-B and induces apoptosis. May play a role in regulating lymphocyte homeostasis.|
|Cellular Location||Isoform 1: Cell membrane; Single-pass type I membrane protein Isoform 9: Cell membrane; Single-pass type I membrane protein Isoform 3: Secreted. Isoform 5: Secreted. Isoform 7: Secreted. Isoform 10: Secreted.|
|Tissue Location||Abundantly expressed in thymocytes and lymphocytes. Detected in lymphocyte-rich tissues such as thymus, colon, intestine, and spleen. Also found in the prostate|
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The protein encoded by this gene is a member of theTNF-receptor superfamily. This receptor is expressed preferentiallyin the tissues enriched in lymphocytes, and it may play a role inregulating lymphocyte homeostasis. This receptor has been shown tostimulate NF-kappa B activity and regulate cell apoptosis. Thesignal transduction of this receptor is mediated by various deathdomain containing adaptor proteins. Knockout studies in micesuggested the role of this gene in the removal of self-reactive Tcells in the thymus. Multiple alternatively spliced transcriptvariants of this gene encoding distinct isoforms have beenreported, most of which are potentially secreted molecules. Thealternative splicing of this gene in B and T cells encounters aprogrammed change upon T-cell activation, which predominantlyproduces full-length, membrane bound isoforms, and is thought to beinvolved in controlling lymphocyte proliferation induced by T-cellactivation.
Bayry, J. Nat Rev Rheumatol 6(2):67-68(2010)Hosgood, H.D. III, et al. Occup Environ Med 66(12):848-853(2009)Andresdottir, M.B., et al. Clin Transplant 23(5):660-665(2009)Fang, L., et al. J. Exp. Med. 205(5):1037-1048(2008)Han, J.Y., et al. Mol. Cells 22(2):168-174(2006)
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