Ultra-LEAF™ Purified anti-mouse IFNgR2 Antibody, IFNgR2, W20010A,BioLegend,671953

Host

Rat

Reactivity

Mouse

Application

Block - Quality tested

Platform ID

BAB521895101

BioLegend

Headquarters

8999 BioLegend Way San Diego, CA 92121 United States

Contact

Tel: 1-858-455-9588
Fax: +49 (4131) 7023913

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Product Specifications
Scientific Background

Specifications

NameUltra-LEAF™ Purified anti-mouse IFNgR2 Antibody, IFNgR2, W20010A
Cat. No.671953
HostRat
RRIDAB_3699086 (BioLegend Cat. No. 671953)AB_3699086 (BioLegend Cat. No. 671954)
IsotypeRat IgG2b, κ
ReactivityMouse
ApplicationBlock - Quality tested
ClonalityMonoclonal
Clone NumberW20010A
ConcentrationThe antibody is bottled at the concentration indicated on the vial, typically between 2 mg/mL and 3 mg/mL. To obtain lot-specific concentration and expiration, please enter the lot number in ourCertificate of Analysisonline tool.
TargetIFNgR2
ImmunogenRecombinant Mouse IFNgR2
PurityThe Ultra-LEAF™ (Low Endotoxin, Azide-Free) antibody was purified by affinity chromatography.
Formulation0.2 µm filtered in phosphate-buffered solution, pH 7.2, containing no preservative.
StorageThe antibody solution should be stored undiluted between 2°C and 8°C. This Ultra-LEAF™ solution contains no preservative; handle under aseptic conditions.
Regulatory StatusResearch Use Only

Scientific Background

IFN-γ initiates and regulates a variety of immune responses. IFNγ receptor is a heterodimer of high affinity IFNγ-binding chain (IFNγR1) and a second accessory protein required for signal transduction known as IFNγR2 (IFN-γ R β chain). IFNγR1 and IFNγR2 belongs to a member of the type II cytokine receptor family. IFNγR1 is constitutively expressed on the surface of T cells, B cells, NK cells, myeloid cells, fibroblasts, endothelial and epithelial cells at the moderate level. IFNγR2 is has low levels of cell surface and high levels of cytoplasmic expression. Though the recycling of IFNγR2 between cell surface and cytoplasm is IFN-γ-independent, it depends on a dipeptide motif on its intracellular domain and its expression is tightly regulated by external stimuli. IFN-γ can decrease mRNA expression of IFNγR2, and modulates T cell responsiveness to IFN-γ. Binding of IFN-γ induces receptor-ligand dimerization, tyrosine phosphorylation of IFNγR1 and internalization. IFNγR2 is resposible for signal transduction, involving Jak1/ Jak2 protein kinases and STAT1 activation. T cells isolated from IFNγR2 deficient mice, or from transgenic mouse (over-expressing IFNγR2) demonstrate impaired capacity to differentiate into the Th1 cells.  Medndelian susceptibility to mycobacterial disease (MSDS) syndrome in human  has been linked to a autosomal recessive and autosomal dominant deficiency of IFNγR2.

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