RIG-I (human), detection set



APO-54N-038-KI01	5x96 wells	554.00 USD

Figure: Good correlation between immunoblotting and ELISA immunoassay in the detection of RIG-I in HeLa cells Method: HeLa cells were treated with interferon-γ for times indicated in the figure. RIG-I present in cell extracts was quantified either by using the RIG-I (human) (IntraCellular) Detection Set [For ELISA Application] (APO-54N-038) or by immunoblotting using MAb to RIG-I (Alme-1) (Prod. No. ALX-804-849).

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Product Specification

Alternative Name:	Retinoic acid-inducible gene 1

Sensitivity:	0.1ng/ml (range 0.156 to 10ng/ml).

Kit/Set Contains:	1 vial Standard (lyophilized) (STD).1 vial Coating Antibody (COAT).1 vial Detection Antibody (DET).

Application:	For the quantitative determination of human intracellular RIG-I in cell extracts.

Short Term Storage:	+4°C

Handling:	Avoid freeze/thaw cycles. For long term storage keep the standard (STD) at -20°C.

Miscellaneous/General:	The innate immune response to viruses is initiated upon detection of viral RNA generated during the life cycle of most viruses [1]. Recognition of the viral RNA is mediated by either the two cytoplasmic RNA helicases Retinoic acid Inducible Gene-1 (RIG-I ; Ddx58) and Melanoma Differentiation Associated gene 5 (MDA5 / Helicard; Ifih1) [2] or by Toll-like Receptor 3 (TLR3) located to an endosomal-like compartment [3]. RIG-I and MDA5 belongs to the family of RIG-I like receptor (RLR) together with the protein LGP2 whose function is still elusive [4, 5]. Upon binding to RNA, RIG-I or MDA5 binds a mediator named Cardif, MAVS (mitochondrial antiviral signalling), IPS-1 (interferon-β promoter stimulator 1), or VISA (virus-induced signalling adapter) [6, 7] that signals through transcription factors, such as IRF-3, IRF-7, and NF-κB leading to the activation of interferons (IFNs) and other inflammatory cytokine genes. RIG-I is activated by dsRNA and 5′-ppp RNA. RIG-I has been shown to trigger innate immune signaling pathways during infection by orthomyxoviruses, rhabdovirus, vesicular stomatitis virus, and paramyxoviruses; and possibly by the filovirus Ebola virus and by the Epstein-Barr virus [8]. Virus infection induces a rapid production of IFN-α/β that leads to expression of hundreds of interferon-stimulated genes (ISGs) whose products direct antiviral actions. RIG-I belongs to the ISG gene family and monitoring its levels using the RIG-I (human) Detection Set (IC) can be used as indicator of IFN production and virus infection.

General Literature References

Cytoplasmic recognition of RNA: M. Yoneyama, et al.; Adv. Drug Deliv. Rev. 60, 841 (2008), Abstract;

Distinct RIG-I and MDA5 signaling by RNA viruses in innate immunity: Y.M. Loo, et al.; J. Virol. 82, 335 (2008), Abstract; Full Text

MDA5/RIG-I and virus recognition: O. Takeuchi & S. Akira; Curr. Opin. Immunol. 20, 17 (2008), Abstract;

TLR3: Interferon induction by double-stranded RNA including poly(I:C): M. Matsumoto & T. Seya; Adv. Drug Deliv. Rev. 60, 805 (2008), Abstract;

Loss of DExD/H box RNA helicase LGP2 manifests disparate antiviral responses: T. Venkataraman, et al.; J. Immunol. 178, 6444 (2007), Abstract; Full Text

Recognition of viruses by innate immunity: O. Takeuchi & S. Akira; Immunol. Rev. 220, 214 (2007), Abstract;

Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus: E. Meylan, et al.; Nature 437, 1167 (2005), Abstract;

IPS-1, an adaptor triggering RIG-I- and Mda5-mediated type I interferon induction: T. Kawai, et al.; Nat. Immunol. 6, 981 (2005), Abstract;