Human TNF Receptor Associated Factor 3 (TRAF3) ELISA Kit
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Description
Human TNF Receptor Associated Factor 3 (TRAF3) ELISA Kit is an ELISA Kit for the in vitro quantitative measurement of Human TRAF3 concentrations in serum, plasma, tissue homogenates, cell lysates and other biological fluids. This assay has high sensitivity and excellent specificity for detection of TNF Receptor Associated Factor 3 (TRAF3)
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Product specifications
| Category | ELISA Kits |
| Immunogen Target | TNF Receptor Associated Factor 3 (TRAF3) |
| Reactivity | Human |
| Detection Method | Colorimetric |
| Assay Data | Quantitative |
| Assay Type | Sandwich |
| Test Range | 15.6 pg/ml - 1000 pg/ml |
| Sensitivity | < 6.1 pg/ml |
| Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
| Size 1 | 96 tests |
| Size 2 | 5 × 96 tests |
| Size 3 | 10 × 96 tests |
| Form | Lyophilized |
| Tested Applications | ELISA |
| Sample Type | Serum, plasma, tissue homogenates, cell lysates and other biological fluids. |
| Availability | Shipped within 5-7 working days. The validity for this kit is at least 6 months. Up to 12 months validity can be provided on request. |
| Storage | Shipped at 4 °C. Upon receipt, store the kit according to the storage instruction in the kit's manual. |
| Dry Ice | No |
| UniProt ID | Q13114 |
| Alias | TRAF-3,TRAF3, CAP-1, CAP1, CD40bp, CRAF1, IIAE5, LAP1, TNF receptor associated factor 3, RNF118 |
| Background | Elisa kits for TRAF3 |
| Status | RUO |
| Note | Validity: The validity for this kit is at least 6 months. Up to 12 months validity can be provided on request. This product is for research use only. The range and sensitivity is subject to change. Please contact us for the latest product information. For accurate results, sample concentrations must be diluted to mid-range of the kit. If you require a specific range, please contact us in advance or write your request in your order comments. Please note that our ELISA and CLIA kits are optimised for detection of native samples, rather than recombinant proteins. We are unable to guarantee detection of recombinant proteins, as they may have different sequences or tertiary structures to the native protein. |
Descripción
TRAF3 is an adaptor protein that regulates signaling downstream of receptors like CD40, BAFF-R, and Toll-like receptors (TLRs), playing a crucial role in immune regulation, lymphocyte activation, and antiviral responses. Unlike TRAF1 and TRAF2, TRAF3 functions as a negative regulator of the non-canonical NF-κB pathway by targeting NIK (NF-κB-inducing kinase) for degradation, thereby preventing constitutive activation of NF-κB2 signaling. TRAF3 is widely expressed in immune cells, where it regulates B-cell survival, interferon production, and immune tolerance. Dysregulation of TRAF3 is associated with B-cell malignancies, autoimmune diseases, and viral infections due to uncontrolled NF-κB activation and impaired immune signaling. Functional studies in knockout models demonstrate defects in B-cell homeostasis, increased susceptibility to autoimmunity, and reduced antiviral immunity, underscoring its dual role in restraining excessive signaling and supporting immune regulation.
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TRAF3 antibody
The protein encoded by this gene is a member of the TNF receptor associated factor (TRAF) protein family. TRAF proteins associate with, and mediate the signal transduction from, members of the TNF receptor (TNFR) superfamily. This protein participates in the signal transduction of CD40, a TNFR family member important for the activation of the immune response. This protein is found to be a critical component of the lymphotoxin-beta receptor (LTbetaR) signaling complex, which induces NF-kappaB activation and cell death initiated by LTbeta ligation. Epstein-Barr virus encoded latent infection membrane protein-1 (LMP1) can interact with this and several other members of the TRAF family, which may be essential for the oncogenic effects of LMP1. Several alternatively spliced transcript variants encoding three distinct isoforms have been reported.
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