TRIAD3 (F1Z2P) Rabbit mAb #65255
- WB
- IP
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | 140 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Immunoprecipitation | 1:200 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
TRIAD3 is a ubiquitin-protein ligase that promotes ubiquitination and proteolytic degradation of multiple TLRs, acting as a negative regulator of their signaling activation (1-4). In addition, TRIAD3 interacts and promotes downregulation of two TIR domain-containing adapter molecules, TIR domain-containing adapter-inducing IFN-β (TRIF) and TRIF-related TIR domain-containing adapter protein (TIRAP) (4). Moreover, TRIAD3 has been shown to act as a negative regulator of TNF-α signaling via its interaction with RIP1, effectively impeding RIP1-mediated NF-κB activation (5).
TRIAD3 has recently been shown to play a role in slowing cardiac hypertrophy by catalyzing ubiquitination-mediated degradation of TLR4 and TLR9, leading to reduced NF-κB pathway activation (6). TRIAD3 has also been shown to mediate autophagy in neurodegenerative diseases. (5,7). In vivo studies show that TRIAD3 decreases the accumulation of phosphorylated tau protein in mouse models. Mutations in TRIAD3 lead to increased accumulation of phosphorylated tau and neurodegenerative disease (7).
- Chuang, T.H. and Ulevitch, R.J. (2004) Nat Immunol 5, 495-502.
- Smit, J.J. and Sixma, T.K. (2014) EMBO Rep 15, 142-54.
- Nakhaei, P. et al. (2009) PLoS Pathog 5, e1000650.
- Fearns, C. et al. (2006) J Biol Chem 281, 34592-600.
- Schwintzer, L. et al. (2019) Cell Death Discov 5, 75.
- Lu, X. et al. (2020) Basic Res Cardiol 115, 19.
- Zhou, J. et al. (2024) Nat Cell Biol 26, 1274-1286.
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