HPA001535
Anti-IFNGR2 antibody produced in rabbit
affinity isolated antibody, buffered aqueous glycerol solution
Synonym(s):
Anti-AF-1 antibody produced in rabbit, Anti-Interferon-γ receptor β-chain precursor antibody produced in rabbit, Anti-Interferon-γ receptor accessory factor 1 antibody produced in rabbit, Anti-Interferon-γ transducer 1 antibody produced in rabbit
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All Photos(4)
About This Item
Recommended Products
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
product line
Prestige Antibodies® Powered by Atlas Antibodies
form
buffered aqueous glycerol solution
species reactivity
human
enhanced validation
orthogonal RNAseq
Learn more about Antibody Enhanced Validation
technique(s)
immunofluorescence: 0.25-2 μg/mL
immunohistochemistry: 1:20-1:50
immunogen sequence
ASPSAGFPMDFNVTLRLRAELGALHSAWVTMPWFQHYRNVTVGPPENIEVTPGEGSLIIRFSSPFDIADTSTAFFCYYVHYWEKGGIQQVKGPFRSNSISLDNLKPSRVYCLQVQAQLLWNKSNIFRVGHLSNIS
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... IFNGR2(3460)
Immunogen
Interferon-γ receptor β-chain precursor recombinant protein epitope signature tag (PrEST)
Application
Anti-IFNGR2 antibody produced in rabbit, a Prestige Antibody, is developed and validated by the Human Protein Atlas (HPA) project . Each antibody is tested by immunohistochemistry against hundreds of normal and disease tissues. These images can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. The antibodies are also tested using immunofluorescence and western blotting. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Immunohistochemistry (1 paper)
Immunohistochemistry (1 paper)
Biochem/physiol Actions
IFNGR2 (interferon γ receptor 2) gene encodes the non-ligand-binding β chain of the γ interferon receptor. The human interferon-γ receptor consists of two subunits IFNGR1 and IFNGR2. This subunit interacts with janus kinase JAK2 and regulates IFN-γ signal transduction pathway. It is involved in interferon-γ mediated immunity. Defects in this gene cause mendelian susceptibility to mycobacterial disease (MSMD), also known as familial disseminated atypical mycobacterial infection.
Features and Benefits
Prestige Antibodies® are highly characterized and extensively validated antibodies with the added benefit of all available characterization data for each target being accessible via the Human Protein Atlas portal linked just below the product name at the top of this page. The uniqueness and low cross-reactivity of the Prestige Antibodies® to other proteins are due to a thorough selection of antigen regions, affinity purification, and stringent selection. Prestige antigen controls are available for every corresponding Prestige Antibody and can be found in the linkage section.
Every Prestige Antibody is tested in the following ways:
Every Prestige Antibody is tested in the following ways:
- IHC tissue array of 44 normal human tissues and 20 of the most common cancer type tissues.
- Protein array of 364 human recombinant protein fragments.
Linkage
Corresponding Antigen APREST78240
Physical form
Solution in phosphate-buffered saline, pH 7.2, containing 40% glycerol and 0.02% sodium azide
Legal Information
Prestige Antibodies is a registered trademark of Merck KGaA, Darmstadt, Germany
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Personal Protective Equipment
dust mask type N95 (US), Eyeshields, Gloves
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Guillaume Vogt et al.
The Journal of experimental medicine, 205(8), 1729-1737 (2008-07-16)
Germline mutations may cause human disease by various mechanisms. Missense and other in-frame mutations may be deleterious because the mutant proteins are not correctly targeted, do not function correctly, or both. We studied a child with mycobacterial disease caused by
Joanna Wesoly et al.
Acta biochimica Polonica, 54(1), 27-38 (2007-03-14)
Interferons (IFNs) induce gene expression by phosphorylating latent transcription factors belonging to the signal transducer and activator of transcription (STAT) family, mediated by janus kinases (Jaks). STAT dimers directly activate genes containing the IFNgamma activation site (GAS) DNA element, with
Jana Ivanidze et al.
The American journal of pathology, 179(3), 1347-1359 (2011-08-23)
Sporadic inclusion body myositis (IBM) is a muscle disease with two separate pathogenic components, degeneration and inflammation. Typically, nonnecrotic myofibers are focally surrounded and invaded by CD8(+) T cells and macrophages. Both attacked and nonattacked myofibers express high levels of
Sofia Roth et al.
PloS one, 11(5), e0154817-e0154817 (2016-05-07)
We previously demonstrated that anthocyanin-rich bilberry extract (ARBE) inhibits IFN-γ-induced signalling and downstream effects in human monocytic cells and ameliorates disease activity in ulcerative colitis (UC) patients. Here, we studied the molecular mechanisms of ARBE-mediated effects in vitro and by
Guillaume Vogt et al.
Nature genetics, 37(7), 692-700 (2005-06-01)
Mutations involving gains of glycosylation have been considered rare, and the pathogenic role of the new carbohydrate chains has never been formally established. We identified three children with mendelian susceptibility to mycobacterial disease who were homozygous with respect to a
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