Thermo Fisher Scientific RNF216 Polyclonal Antibody

Applications

Tested Dilution

Publications

Immunohistochemistry (Paraffin) (IHC (P))

1:50-1:200

-

Immunocytochemistry (ICC/IF)

0.25-2 µg/mL

-

Product Specifications

Species Reactivity

Human

Host/Isotype

Rabbit / IgG

Class

Polyclonal

Type

Antibody

Immunogen

Recombinant protein corresponding to Human RNF216. Recombinant protein control fragment (Product #RP-92071). if (typeof window.$mangular === undefined || !window.$mangular) { window.$mangular = {}; } $mangular.antigenJson = \[{targetFamily:RNF216,uniProtId:Q9NWF9-2,ncbiNodeId:9606,antigenRange:288-367,antigenLength:866,antigenImageFileName:PA5-82649_RNF216_Q9NWF9-2_Rabbit.svg,antigenImageFileNamePDP:PA5-82649_RNF216_Q9NWF9-2_Rabbit_PDP.jpeg,sortOrder:1}\]; $mangular.isB2BCMGT = false; $mangular.isEpitopesModalImageMultiSizeEnabled = true;

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Conjugate

Unconjugated Unconjugated Unconjugated

Form

Liquid

Concentration

0.05 mg/mL

Purification

Antigen affinity chromatography

Storage buffer

PBS, pH 7.2, with 40% glycerol

Contains

0.02% sodium azide

Storage conditions

Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.

Shipping conditions

Wet ice

RRID

AB_2789805

Product Specific Information

Immunogen sequence: VKETEARFPD VANGFIEEII HFKNYYDLNV LCNFLLENPD YPKREDRIII NPSSSLLASQ DETKLPKIDF FDYSKLTPLD

Target Information

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.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.