ELISA. Western blot: 0.5 to 1 μg/mL. Immunohistochemistry on paraffin sections. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user.
Beschränkungen
Nur für Forschungszwecke einsetzbar
Buffer
PBS containing 0.02 % sodium azide
Konservierungsmittel
Sodium azide
Vorsichtsmaßnahmen
This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Handhabung
Avoid repeated freezing and thawing.
Lagerung
4 °C/-20 °C
Informationen zur Lagerung
Store at 2 - 8 °C for up to one month or (in aliquots) at -20 °C for longer.
Activation of NF-kappaB as a result of Toll-like receptor (TLR) and IL-1 receptor signaling is a major component of innate immune responses (reviewed in 1). Signals from these receptors are relayed by a number of adapter molecules such as TRIF, TIRAP, and MyD88 (2). Several regulatory mechanisms exist to control TLR signal transduction, including the inhibition of TLR expression and signaling by molecules such as ST2 and SIGIRR (3,4). Another mechanism is by the ubi-quitinization of selected TLRs by TRIAD3A, an E3 ubiquitin-protein ligase (5). 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 (5).Synonyms: E3 ubiquitin-protein ligase RNF216, RING finger protein 216, TRIAD3, Triad domain-containing protein 3, UBCE7IP1, Ubiquitin-conjugating enzyme 7-interacting protein 1, ZIN, Zinc finger protein inhibiting NF-kappa-B