VISA / MAVS Antibody (Internal)
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application ![]()
| WB, IHC-P |
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Primary Accession | Q7Z434 |
Reactivity | Human, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Calculated MW | 57kDa |
Dilution | IHC-P (5 µg/ml), WB (0.5-2 µg/ml), |
Gene ID | 57506 |
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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 | 17 amino acid peptide from near the center of human VISA. |
Reconstitution & Storage | Short term 4°C, long term aliquot and store at -20°C, avoid freeze thaw cycles. Store undiluted. |
Precautions | VISA / MAVS Antibody (Internal) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | MAVS {ECO:0000303|PubMed:16125763, ECO:0000312|HGNC:HGNC:29233} |
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Function | Adapter required for innate immune defense against viruses (PubMed:16125763, PubMed:16127453, PubMed:16153868, PubMed:16177806, PubMed:19631370, PubMed:20127681, PubMed:20451243, PubMed:21170385, PubMed:23087404, PubMed:27992402, PubMed:33139700, PubMed:37582970). Acts downstream of DHX33, RIGI 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 IFNB and RANTES (CCL5) (PubMed:16125763, PubMed:16127453, PubMed:16153868, PubMed:16177806, PubMed:19631370, PubMed:20127681, PubMed:20451243, PubMed:20628368, PubMed:21170385, PubMed:23087404, PubMed:25636800, PubMed:27736772, PubMed:33110251). Peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state (PubMed:20451243). 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 (PubMed:20451243). May activate the same pathways following detection of extracellular dsRNA by TLR3 (PubMed:16153868). May protect cells from apoptosis (PubMed:16125763). Involved in NLRP3 inflammasome activation by mediating NLRP3 recruitment to mitochondria (PubMed:23582325). |
Cellular Location | Mitochondrion outer membrane; Single-pass membrane protein. 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.
Background
Required for innate immune defense against viruses. Acts downstream of 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.
References
Seth R.B.,et al.Cell 122:669-682(2005).
Xu L.-G.,et al.Mol. Cell 19:727-740(2005).
Meylan E.,et al.Nature 437:1167-1172(2005).
Kawai T.,et al.Nat. Immunol. 6:981-988(2005).
Lad S.P.,et al.Mol. Immunol. 45:2277-2287(2008).

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