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TNFRSF25 (tumor necrosis factor receptor superfamily, member 25) Blocking Peptide (the middle region of protein) (100ug)

TNFRSF25 (tumor necrosis factor receptor superfamily, member 25) Blocking Peptide (the middle region of protein) (100ug)

Supplier: Aviva Systems Biology Incorporated
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This is a synthetic peptide designed for use in combination with anti-TNFRSF25 antibody (Catalogue #: AVARP02066_P050) made by Aviva Systems Biology. It may block above mentioned antibody from binding to its target protein in western blot and/or immunohistochecmistry under proper experimental settings. There is no guarantee for its use in other applications. Please inquire for more details.
Presku: AAP30625
Size: 100 ug
Weight: 38kDa
Gene: 8718
Format: Lyophilized powder
Target: TNFRSF25 is a member of the TNF-receptor superfamily. This receptor is expressed preferentially in the tissues enriched in lymphocytes, and it may play a role in regulating lymphocyte homeostasis. This receptor has been shown to stimulate NF-kappa B activity and regulate cell apoptosis. The signal transduction of this receptor is mediated by various death domain containing adaptor proteins. Knockout studies in mice suggested the role of this gene in the removal of self-reactive T cells in the thymus. Multiple alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported, most of which are potentially secreted molecules. The alternative splicing of this gene in B and T cells encounters a programmed change upon T-cell activation, which predominantly produces full-length, membrane bound isoforms, and is thought to be involved in controlling lymphocyte proliferation induced by T-cell activation.The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor is expressed preferentially in the tissues enriched in lymphocytes, and it may play a role in regulating lymphocyte homeostasis. This receptor has been shown to stimulate NF-kappa B activity and regulate cell apoptosis. The signal transduction of this receptor is mediated by various death domain containing adaptor proteins. Knockout studies in mice suggested the role of this gene in the removal of self-reactive T cells in the thymus. Multiple alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported, most of which are potentially secreted molecules. The alternative splicing of this gene in B and T cells encounters a programmed change upon T-cell activation, which predominantly produces full-length, membrane bound isoforms, and is thought to be involved in controlling lymphocyte proliferation induced by T-cell activation.
Alternative names: APO-3; DDR3; DR3; LARD; TNFRSF12; TR3; TRAMP; WSL-1; WSL-LR
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