Recombinant Mouse Mitochondrial antiviral-signaling protein (Mavs), partial

Code CSB-YP844990MO
MSDS
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Source Yeast
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Code CSB-EP844990MO
MSDS
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Source E.coli
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Code CSB-EP844990MO-B
MSDS
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Source E.coli
Conjugate Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
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Code CSB-BP844990MO
MSDS
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Source Baculovirus
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Code CSB-MP844990MO
MSDS
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Source Mammalian cell
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Product Details

Purity
>85% (SDS-PAGE)
Target Names
Uniprot No.
Alternative Names
Mavs; Ips1; Visa; Mitochondrial antiviral-signaling protein; MAVS; CARD adapter inducing interferon beta; Cardif; Interferon beta promoter stimulator protein 1; IPS-1; Virus-induced-signaling adapter; VISA
Species
Mus musculus (Mouse)
Protein Length
Partial
Tag Info
Tag type will be determined during the manufacturing process.
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
Form
Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer before Lyophilization
Tris/PBS-based buffer, 6% Trehalose.
Reconstitution
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Notes
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet
Please contact us to get it.

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Target Background

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.
Gene References into Functions
  1. Data show that interferon-beta promotor stimulator-1 (IPS-1) deficiency predisposed to severe pneumonia virus of mice (PVM) bronchiolitis. PMID: 28539639
  2. MAVS deficiency is associated with allergic skin disease. PMID: 30249647
  3. these data suggest that while MAVS signaling has a considerable impact on Treg identity, this effect is not mediated by intrinsic MAVS signaling but rather is likely an effect of the overproduction of pro-inflammatory cytokines generated in MAVS-deficient mice after WNV infection. PMID: 28094802
  4. MAVS was identified as a main player in HDV detection and adaptive immunity was found to be involved in the amplification of the innate immune response. PMID: 28527664
  5. MAVS is essential for spontaneous high basal expression of IFN-beta in cardiac myocytes and the heart. PMID: 28822807
  6. findings suggest that oxidative stress-induced MAVS oligomerization in SLE patients may contribute to the type I IFN signature that is characteristic of this syndrome. PMID: 27899525
  7. this study shows that keratinocytes are an important source of IFN-beta and MAVS is critical to this function, and demonstrates how the epidermis triggers unwanted skin inflammation under disease conditions PMID: 27438769
  8. RIPK3 regulates type I IFN both transcriptionally, by interacting with MAVS and limiting RIPK1 interaction with MAVS, and post-transcriptionally. PMID: 28410401
  9. Taken together, these results suggest that MAVS is essential for boosting optimal primary CD4(+) T cell responses upon NS4B-P38G West Nile virus vaccination and yet is dispensable for host protection and recall T cell responses during secondary wild-type West Nile virus infection. PMID: 28077630
  10. this study demonstrates that the capacity of hepatitis A virus to evade MAVS-mediated type I interferon responses defines its host species range. PMID: 27633528
  11. Hepatitis C virus NS3-4A inhibits the peroxisomal MAVS-dependent antiviral signaling response. PMID: 26865163
  12. An autoinhibitory mechanism modulates MAVS activity in unstimulated cells and, on viral infection, individual regions of MAVS are released following MAVS filament formation to activate antiviral signalling cascades. PMID: 26183716
  13. indicate comparable activation of the IFN response by pex- and mito-mitochondrial antiviral-signaling protein in hepatocytes and efficient counteraction of both MAVS species by the HCV nonstructural protein 3 protease PMID: 26588843
  14. Transmembrane motif T6BM2-mediated TRAF6 binding is required for MAVS-related antiviral response. PMID: 26385923
  15. Data show that intracellular adaptor protein Cardif-/- natural killer cells (NK cells) are more apoptotic and less proliferative. PMID: 26232430
  16. Elucidate the structural mechanism of MAVS polymerization, and explain how an alpha-helical domain uses distinct chemical interactions to form self-perpetuating filaments. PMID: 24569476
  17. MAVS plays an essential role in host immunity against metapneumovirus infection. PMID: 25953917
  18. results indicate that Lyn plays a positive regulatory role in RIG-I-mediated interferon expression as a downstream component of IPS-1 PMID: 25585356
  19. In lung epithelial cells, retinoic acid-inducible gene-1 (RIG-I) was identified as the major RIG-I-like receptor required for RSV-induced protease expression via MAVS. PMID: 25005357
  20. This study has identified a previously unrecognized role of MAVS in the regulation of inflammasome signaling PMID: 25847972
  21. These results establish a dominant protective role for MAVS, IRF-3 and IRF-7, and IFNAR in restricting Oropouche virus infection and tissue injury and suggest that IFN signaling in nonmyeloid cells contributes to the host defense. PMID: 25717109
  22. findings demonstrate that IFN-beta, but not IFN-lambda2/3, produced via an IPS-1-IRF3 signaling pathway, is important for hMPV clearance. PMID: 24726644
  23. Deficient IFN signaling by myeloid cells leads to MAVS-dependent virus-induced sepsis. PMID: 24743949
  24. that Smurf2 is an important nonredundant negative regulator of virus-triggered type I IFN signaling by targeting VISA for K48-linked ubiquitination and degradation. PMID: 24729608
  25. Data indicate that IPS-1-dependent pathway plays a crucial role in type III IFN production by CD8(+) dendritic cells (DCs) and hepatocytes in response to hepatitis C virus (HCV), leading to cytoplasmic antiviral protein expressions. PMID: 24532585
  26. In virus-infected cells, a Bax/Bak-independent pathway involves dsRNA-induced innate immune signaling via mitochondrial antiviral signaling (MAVS) and caspase-8. PMID: 24391214
  27. MAVS participates in the initial induction of type I IFN in bone marrow-derived dendritic cells and IFNAR protects against MV spreading. PMID: 24096085
  28. data suggest that IPS-1 plays a dual function in inducing murine melanoma B16F10 cell apoptosis PMID: 23784981
  29. MAVS binds to voltage-dependent anion channel 1 (VDAC1) and induces apoptosis by caspase-3 activation, which is independent of its role in innate immunity. PMID: 23754752
  30. La Crosse virus infection induced the RNA helicase, RIG-I, and mitochondrial antiviral signaling protein (MAVS) signaling pathway, resulting in upregulation of the sterile alpha and TIR-containing motif 1 (SARM1), an adaptor molecule that we found to be directly involved in neuronal damage PMID: 23499490
  31. IPS-1 is essential for protection and control of an attenuated Sindbis virus. PMID: 23084425
  32. Viral clearance and inflammation resolution are strongly affected by the absence of an initial IPS-1-mediated interferon (IFN)-beta response. PMID: 23136205
  33. novel residue of MAVS that is crucially involved in the recruitment of TRAF3/TRAF6 and in downstream propagation of MAVS signaling PMID: 22844514
  34. UXT-V1 represents a novel integral component of the MAVS signalosome on mitochondria, mediating the innate antiviral signal transduction. PMID: 22131337
  35. Bone marrow transplantation experiments revealed that MAVS in cells of nonhematopoietic origin plays a dominant role in the protection against colitis. PMID: 21960441
  36. found that PB1-F2 inhibited IFN production at the level of the mitochondrial antiviral signaling protein PMID: 21695240
  37. Viral infection induces the formation of very large MAVS aggregates, which potently activate IRF3 in the cytosol; results suggest that a prion-like conformational switch of MAVS activates and propagates the antiviral signaling cascade. PMID: 21782231
  38. Regulation of Igh-1b (RIG-I) or melanoma differentiation-associated (MDA)5 signaling through MAVS is required for activation of interferon (IFN)-beta production by rotavirus-infected intestinal epithelium. PMID: 21187438
  39. these results showed that conjunctival epithelial cells express RIG-I and MDA5, and IPS-1, an adaptor molecule common to RIG-I and MDA5, contributes to polyI:C-inducible cytokine production in conjunctival epithelial cells. PMID: 21130742
  40. gammaHV68 hijacks the antiviral MAVS-IKKbeta pathway to promote viral transcription and lytic infection, whereby viral replication is coupled to host immune activation PMID: 20686657
  41. IPS-1 is essential for both bone marrow derived DC activation and IFN production in rabies PMID: 20661430
  42. Our data define an innate/adaptive immune interface mediated through IPS-1-dependent RIG-I-like receptor signaling in response to West Nile virus infection PMID: 20140199
  43. show that interferon-beta promoter stimulator 1 (IPS-1) binds DAP3 and induces anoikis by caspase activation. PMID: 19644511
  44. The overexpression of mitochondrial antiviral signaling(MAVS)induces the expression of IFN-beta through activation of NF-kappaB and IRF 3, thus boosting antiviral immunity. PMID: 16125763
  45. Data suggest that VISA is critically involved in both virus-triggered TLR3-independent and TLR3-mediated antiviral interferon signaling. PMID: 16153868
  46. IPS-1 is the sole adapter in both retinoic acid-inducible gene (RIG-I) and melanoma differentiation-associated gene 5 (Mda5) signaling that mediates effective responses against a variety of RNA viruses. PMID: 16785313
  47. These results define IPS-1-dependent signaling as an essential feature of host immunity to RNA virus infection. PMID: 17942531
  48. RIG-1 - MAVS interacts with cytoplasmic 100-kDa NF-kappa B2 complexes via a novel retinoic acid-inducible gene-I - NF- kappa B-inducing kinase signaling pathway PMID: 18550535
  49. provide an example of a normal and effective adaptive immune response in the absence of innate immunity mediated by MAVS and MyD88 PMID: 18780793
  50. Upon Sendai virus (SeV) infection, TBK1s is induced in both human and mouse cells and binds to RIG-1, disrupting the interaction between RIG-I and VISA PMID: 18977754

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Subcellular Location
Mitochondrion outer membrane. Mitochondrion. Peroxisome.
Database Links
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