TRAF5 antibody
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Name
TRAF5 antibody
Category
Primary Antibodies
Provider
FineTest
Reference
FNab08920
Tested Applications
ELISA, WB, IHC
Description
Adapter protein and signal transducer that links members of the tumor necrosis factor receptor family to different signaling pathways by association with the receptor cytoplasmic domain and kinases. Mediates activation of NF-kappa-B and probably JNK. Seems to be involved in apoptosis. Plays a role in mediating activation of NF-kappa-B by EIF2AK2/PKR.
Documentos del producto
Especificaciones del producto
| Category | Primary Antibodies |
| Immunogen Target | TNF receptor-associated factor 5 (TRAF5) |
| Host | Rabbit |
| Reactivity | Human, Rat |
| Recommended Dilution | WB: 1:500 - 1:2000; IHC: 1:50 - 1:500 |
| Clonality | polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Observed MW | 64 kDa |
| Purity | ≥95% as determined by SDS-PAGE |
| Purification | Immunogen affinity purified |
| Size 1 | 100µg |
| Form | liquid |
| Tested Applications | ELISA, WB, IHC |
| Storage | PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.) |
| UniProt ID | O00463 |
| Gene ID | 7188 |
| Alias | TRAF-5,TRAF5, MGC:39780, RNF84, TNF receptor associated factor 5 |
| Background | Antibody anti-TRAF5 |
| Status | RUO |
| Note | Mol. Weight 64 kDa |
Background
TRAF5 is a signaling adaptor protein that mediates pathways downstream of TNF receptors (TNFR), CD40, and BAFF-R, activating NF-κB and JNK to regulate inflammation, immune cell activation, and survival. TRAF5 plays a critical role in adaptive immune responses, particularly in T and B cell activation, cytokine production, and lymphoid tissue development. It works redundantly with TRAF2 to promote canonical NF-κB activation, ensuring appropriate immune responses to inflammatory and survival signals. TRAF5 is widely expressed in immune cells and epithelial tissues, where it supports cellular signaling during infections and tissue repair. Dysregulation of TRAF5 contributes to autoimmune diseases and inflammatory conditions, where altered NF-κB signaling enhances cytokine production and immune cell proliferation. Knockout studies reveal defects in lymphocyte activation, impaired cytokine signaling, and altered immune responses, highlighting its importance in immune regulation and inflammatory signaling.
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