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Validated All-in-One™ qPCR Primer for TNFRSF25(NM_148965.1) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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. [provided by RefSeq].
Gene References into function
- These data confirm that silencer of death domains (SODD) and death receptor 3 (DR3) are expressed in a regulated manner during renal transplant rejection, and identify DR3 as a potential inducible mediator of tubular inflammation and injury.
- TL1A-induced NF-kappaB activation and c-IAP2 production prevent DR3-mediated apoptosis
- Death receptor 3 gene duplication is associated with rheumatoid arthritis
- TL1A and DR3 is involved in atherosclerosis via the induction of pro-inflammatory cytokines/chemokines
- VEGI gene expression is subject to regulation by inflammatory cytokines. VEGI is also able to regulate the expression of several important genes involved in angiogenesis.
- Results suggest that death receptor-3 activation can mediate apoptosis in osteoblasts, although its activity is highly restricted by its soluble ligand-binding isoform and possibly also by alternate survival signals.
- These results suggest that caspase-10, DR-3 and IGFBP-3 are involved in apoptosis in the preeclamptic placenta.
- TNFR25/TL1A pair provides an early signal for cytokine production in the lung, and therefore may be a drug target in attempts to attenuate lung inflammation in asthmatics.
