AdipoGen Life Sciences

anti-Cardif (human), mAb (Adri-1)

CHF 460.00
In stock
AG-20B-0004-C100100 µgCHF 460.00
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Product Details
Synonyms CARD Adapter Inducing Interferon-β; IPS-1; MAVS; Mitochondrial Antiviral Signaling Protein; VISA; Virus-induced Signaling Adapter; Interferon-β Promoter Stimulator Protein 1
Product Type Monoclonal Antibody
Properties
Clone Adri-1
Isotype Mouse IgG2b
Source/Host Purified from concentrated hybridoma tissue culture supernatant.
Immunogen/Antigen Recombinant human Cardif (aa 160-450).
Application

Immunocytochemistry: (1:100)
Immunohistochemistry: (paraffin sections)
Immunoprecipitation: (1:200)
Western Blot: (1:1’000)

Crossreactivity Human
Specificity

Recognizes human Cardif.

Purity ≥95% (SDS-PAGE)
Purity Detail Protein G-affinity purified.
Concentration 1mg/ml
Formulation Liquid. In PBS containing 10% glycerol and 0.02% sodium azide.
Isotype Negative Control

Mouse IgG2b Isotype Control

Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage -20°C
Handling Advice After opening, prepare aliquots and store at -20°C.
Avoid freeze/thaw cycles.
Use/Stability Stable for at least 1 year after receipt when stored at -20°C.
Documents
MSDS Download PDF
Product Specification Sheet
Datasheet Download PDF
Description

RIG-I (retinoic acid-inducible gene I; Ddx58) and MDA5 (melanoma differentiation-associated gene 5, also known as Ifih1 or Helicard) are proteins that sense viral replication intermediates, such as double-stranded RNA and triggers the host antiviral programs. These molecules signal the downstream activation of NF-κB and IFN regulatory factor (IRF) -3, which coordinately regulate the expression of type-I interferons. Cardif (also called VISA/IPS-1/MAVS) is a new CARD (caspase activation and recruitment domain)-containing adaptor protein that interacts with the CARD domain of RIG-I and MDA5, leading to the activation of NF-κB and IRF3. Cardif is located to the mitochondrial outer membrane. Removal of the mitochondrial-targeting domain of cardif abolishes its ability to induce IFNs. Cardif is cleaved and inactivated by NS3-4A, a serine protease from hepatitis C virus known to block interferon-β production.

Product References
  1. TRADD Protein Is an Essential Component of the RIG-like Helicase Antiviral Pathway: M.C. Michallet, et al.; Immunity 28, 651 (2008)
  2. Cleavage of mitochondrial antiviral signaling protein in the liver of patients with chronic hepatitis C correlates with a reduced activation of the endogenous interferon system: P. Bellecave, et al.; Hepatology 51, 1127 (2010)
  3. Quantitative proteomics identifies the membrane-associated peroxidase GPx8 as a cellular substrate of the hepatitis C virus NS3-4A protease: K. Morikawa, et al.; Hepatology 59, 423 (2014)
  4. Hepatitis C virus variants resistant to macrocyclic NS3-4A inhibitors subvert IFN-β induction by efficient MAVS cleavage: C. Welsch, et al.; J. Hepatol. 62, 779 (2015)
  5. Extended interaction networks with HCV protease NS3-4A substrates explain the lack of adaptive capability against protease inhibitors: G. Dultz, et al.; J. Biol. Chem. 295, 13862 (2020)
  6. Deficiency in coatomer complex I causes aberrant activation of STING signalling: A. Steiner, et al.; Nature Comm. 13, 2321 (2022)
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