|Application ||WB, IHC-P, IF, E|
|Other Accession||AAP47174, 54476|
|Calculated MW||99406 Da|
|Application Notes||TRIAD3A antibody can be used for detection of TRIAD3A by Western blot at 1 to 2 μg/mL. Antibody can also be used for immunohistochemistry starting at 10 μg/mL. For immunofluorescence start at 20 μg/mL.|
|Other Names||TRIAD3A Antibody: ZIN, CAHH, U7I1, TRIAD3, UBCE7IP1, ZIN, E3 ubiquitin-protein ligase RNF216, RING finger protein 216, ring finger protein 216|
|Target/Specificity||TRIAD3A antibody was raised against a peptide corresponding to 15 amino acids near the amino-terminus of mouse TRIAD3A.|
The immunogen is located within amino acids 120 - 170 of TRIAD3A.
|Reconstitution & Storage||TRIAD3A antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||TRIAD3A Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||TRIAD3, UBCE7IP1, ZIN|
|Function||Isoform 1 acts as an E3 ubiquitin ligase, which accepts ubiquitin from specific E2 ubiquitin-conjugating enzymes, and then transfers it to substrates promoting their degradation by the proteasome. Promotes degradation of TRAF3, TLR4 and TLR9. Contributes to the regulation of antiviral responses. Down- regulates activation of NF-kappa-B, IRF3 activation and IFNB production. Isoform 3 inhibits TNF and IL-1 mediated activation of NF-kappa-B. Promotes TNF and RIP mediated apoptosis.|
|Tissue Location||Ubiquitous, with the highest levels of expression in testis and peripheral blood leukocytes|
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Provided below are standard protocols that you may find useful for product applications.
TRIAD3A Antibody: Activation of NF-κB as a result of Toll-like receptor (TLR) and IL-1 receptor signaling is a major component of innate immune responses. Signals from these receptors are relayed by a number of adapter molecules such as TRIF, TIRAP, and MyD88. Several regulatory mechanisms exist to control TLR signal transduction, including the inhibition of TLR expression and signaling by molecules such as ST2 and SIGIRR. Another mechanism is by the ubi-quitinization of selected TLRs by TRIAD3A, an E3 ubiquitin-protein ligase. TRIAD3A is a RING finger protein that can bind to TLR4 and TLR9, and to a lesser extent TLR3 and TLR5, catalyzing the ubiquitization of these molecules. Overexpression of TRIAD3A promoted the nearly complete degradation of TLR4 and TLR9; this reduction was reflected in the decreased signal-specific activation by ligands specific for these TLRs. Conversely, depletion of TRIAD3A resulted in enhanced TLR activation.
Takeda K, Kaisho T, and Akira S. Toll-like receptors. Annu. Rev. Immunol. 2003; 21:335-76.
Vogel SN, Fitzgerald KA, and Fenton MJ. TLRs: differential adapter utilization by toll-like receptors mediates TLR-specific patterns of gene expression. Mol. Interv. 2003; 3:466-77.
Sweet MJ, Leung BP, Kang D, et al. A novel pathway regulating lipopolysaccharide-induced shock by ST2/T1 via inhibition of Toll-like receptor 4 expression. J. Immunol. 2001; 166:6633-9.
Wald D, Qin J, Zhao Z, et al. SIGIRR, a negative regulator of Toll-like receptor-interleukin 1 receptor signaling. Nat. Immunol. 2003; 4:920-7.
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