TNFRSF25
TNFRSF25 (tumour necrosis factor receptor superfamily member 25, also known as DR3, TRAMP, WSL-1, LARD, APO-3 and TNFRSF12) is a death domain-containing receptor for TWEAK (TNFSF12). It activates NF-kappa-B, induces apoptosis and is thought to help regulate lymphocyte homeostasis. Browse Assay Genie's current range of TNFRSF25 research reagents below, or read on for the biology behind the target.
TNFRSF25 is a receptor for TNFSF12, also called APO3L or TWEAK. It interacts directly with the adapter protein TRADD, and its signal transduction is mediated by various death domain-containing adaptor proteins. Through this signalling, TNFRSF25 mediates activation of NF-kappa-B and induces apoptosis. It is thought to play a role in regulating lymphocyte homeostasis.
The TNFRSF25 gene encodes a member of the TNF receptor superfamily. The receptor is expressed preferentially in tissues enriched in lymphocytes. Knockout studies in mice suggested a role for the gene in the removal of self-reactive T cells in the thymus. The protein is found at the cell membrane and in a secreted form.
Multiple alternatively spliced transcript variants encode distinct isoforms, and most are potentially secreted molecules. Splicing in B and T cells undergoes a programmed change upon T-cell activation, which predominantly yields full-length, membrane-bound isoforms. This shift is thought to be involved in controlling lymphocyte proliferation induced by T-cell activation. The receptor has also been catalogued under the names DR3, TRAMP, WSL-1, LARD, WSL-LR, DDR3, TR3 and APO-3, and the earlier symbol TNFRSF12 (translocating chain-association membrane protein).
TNFRSF25 is expressed preferentially in lymphocyte-rich tissues and may regulate lymphocyte homeostasis.
The receptor engages TRADD and other death domain adaptors to drive apoptosis, making it a model for studying TNF superfamily signalling.
TNFRSF25 stimulates NF-kappa-B activity, linking TWEAK binding to downstream transcriptional responses.
Mouse knockout studies suggest a role in removing self-reactive T cells in the thymus, and splicing shifts upon T-cell activation.
TNFRSF25 is a receptor for TNFSF12 (TWEAK). It binds the adapter TRADD, activates NF-kappa-B and induces apoptosis. It is also thought to help regulate lymphocyte homeostasis, and mouse knockout studies point to a role in removing self-reactive T cells in the thymus.
TNFRSF25 is also known as DR3, TRAMP, WSL-1, LARD, WSL-LR, DDR3, TR3, APO-3 and, previously, TNFRSF12. Alternative splicing produces multiple isoforms, most of them potentially secreted. Upon T-cell activation, splicing predominantly yields full-length, membrane-bound forms.
Yes. The receptor is expressed preferentially in lymphocyte-enriched tissues, and its splicing in B and T cells changes on T-cell activation. This is thought to help control activation-induced lymphocyte proliferation. Check the datasheet of any product for its validated reactivity.
Other members of the TNF receptor superfamily with research reagents at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q93038; product specifications from Assay Genie datasheets.