|Other Names||Mitochondrial antiviral-signaling protein, MAVS, CARD adapter inducing interferon beta, Cardif, Interferon beta promoter stimulator protein 1, IPS-1, Putative NF-kappa-B-activating protein 031N, Virus-induced-signaling adapter, VISA, MAVS, IPS1, KIAA1271, VISA|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP13783b was selected from the C-term region of MAVS. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Required for innate immune defense against viruses. Acts downstream of DHX33, DDX58/RIG-I and IFIH1/MDA5, which detect intracellular dsRNA produced during viral replication, to coordinate pathways leading to the activation of NF-kappa-B, IRF3 and IRF7, and to the subsequent induction of antiviral cytokines such as IFN-beta and RANTES (CCL5). Peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state. Upon viral infection, peroxisomal MAVS induces the rapid interferon- independent expression of defense factors that provide short-term protection, whereas mitochondrial MAVS activates an interferon- dependent signaling pathway with delayed kinetics, which amplifies and stabilizes the antiviral response. May activate the same pathways following detection of extracellular dsRNA by TLR3. May protect cells from apoptosis.|
|Cellular Location||Mitochondrion outer membrane. Mitochondrion Peroxisome|
|Tissue Location||Present in T-cells, monocytes, epithelial cells and hepatocytes (at protein level). Ubiquitously expressed, with highest levels in heart, skeletal muscle, liver, placenta and peripheral blood leukocytes.|
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Provided below are standard protocols that you may find useful for product applications.
Double-stranded RNA viruses are recognized in a celltype-dependent manner by the transmembrane receptor TLR3 (MIM603029) or by the cytoplasmic RNA helicases MDA5 (MIM 606951) andRIGI (ROBO3; MIM 608630). These interactions initiate signalingpathways that differ in their initial steps but converge in theactivation of the protein kinases IKKA (CHUK; MIM 600664) and IKKB(IKBKB; MIM 603258), which activate NFKB (see MIM 164011), or TBK1(MIM 604834) and IKKE (IKBKE; MIM 605048), which activate IRF3 (MIM603734). Activated IRF3 and NFKB induce transcription of IFNB(IFNB1; MIM 147640). For the TLR3 pathway, the intermediarymolecule before the pathways converge is the cytoplasmic proteinTRIF (TICAM1; MIM 607601). For RIGI, the intermediary protein ismitochondria-bound IPS1 (Sen and Sarkar, 2005 [PubMed16239922]).
Sebastiani, P., et al. Science (2010) In press :Wang, X., et al. Cell. Mol. Immunol. 7(5):341-348(2010)Graef, K.M., et al. J. Virol. 84(17):8433-8445(2010)Wei, C., et al. J. Immunol. 185(2):1158-1168(2010)Onoguchi, K., et al. PLoS Pathog. 6 (7), E1001012 (2010) :
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