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Mouse Anti-IFNGR1 Recombinant Antibody (CBYY-I0808) (CBMAB-I1800-YY)

This product is Mouse antibody that recognizes IFNGR1. The antibody CBYY-I0808 can be used for immunoassay techniques such as: WB, FC, Neut, CyTOF
See all IFNGR1 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBYY-I0808
Antibody Isotype
IgG1
Application
WB, FC, Neut, CyTOF

Basic Information

Specificity
Human
Antibody Isotype
IgG1
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Concentration
0.2 mg/ml
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
interferon gamma receptor 1
Introduction
This gene (IFNGR1) encodes the ligand-binding chain (alpha) of the gamma interferon receptor. Human interferon-gamma receptor is a heterodimer of IFNGR1 and IFNGR2. A genetic variation in IFNGR1 is associated with susceptibility to Helicobacter pylori infection. In addition, defects in IFNGR1 are a cause of mendelian susceptibility to mycobacterial disease, also known as familial disseminated atypical mycobacterial infection.
Entrez Gene ID
3459
UniProt ID
P15260
Alternative Names
Interferon Gamma Receptor 1
Function
Receptor subunit for interferon gamma/INFG that plays crucial roles in antimicrobial, antiviral, and antitumor responses by activating effector immune cells and enhancing antigen presentation (PubMed:20015550).

Associates with transmembrane accessory factor IFNGR2 to form a functional receptor (PubMed:7615558, PubMed:2971451, PubMed:7617032, PubMed:10986460, PubMed:7673114).

Upon ligand binding, the intracellular domain of IFNGR1 opens out to allow association of downstream signaling components JAK1 and JAK2. In turn, activated JAK1 phosphorylates IFNGR1 to form a docking site for STAT1. Subsequent phosphorylation of STAT1 leads to dimerization, translocation to the nucleus, and stimulation of target gene transcription (PubMed:28883123).

STAT3 can also be activated in a similar manner although activation seems weaker. IFNGR1 intracellular domain phosphorylation also provides a docking site for SOCS1 that regulates the JAK-STAT pathway by competing with STAT1 binding to IFNGR1 (By similarity).
Biological Process
Astrocyte activation Source: ARUK-UCL
Cytokine-mediated signaling pathway Source: GO_Central
Defense response to virus Source: Ensembl
Microglial cell activation Source: ARUK-UCL
Negative regulation of amyloid-beta clearance Source: ARUK-UCL
Positive regulation of amyloid-beta formation Source: ARUK-UCL
Positive regulation of gene expression Source: ARUK-UCL
Positive regulation of tumor necrosis factor production Source: ARUK-UCL
Response to virus Source: ProtInc
Signal transduction Source: ProtInc
Cellular Location
Cell membrane
Involvement in disease
Immunodeficiency 27A (IMD27A):
A form of Mendelian susceptibility to mycobacterial disease, a rare condition caused by impairment of interferon-gamma mediated immunity. It is characterized by predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine, environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. Clinical outcome severity depends on the degree of impairment of interferon-gamma mediated immunity. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas.
Immunodeficiency 27B (IMD27B):
A form of Mendelian susceptibility to mycobacterial disease, a rare condition caused by impairment of interferon-gamma mediated immunity. It is characterized by predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine, environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. Clinical outcome severity depends on the degree of impairment of interferon-gamma mediated immunity. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. IMD27B commonly presents with recurrent, moderately severe infections with environmental mycobacteria or BCG. Salmonellosis is present in about 5% of patients.
Topology
Extracellular: 18-245
Helical: 246-266
Cytoplasmic: 267-489
PTM
Phosphorylated at Ser/Thr residues. Phosphorylation of Tyr-457 is required for IFNG receptor signal transduction (PubMed:8156998). Influenza virus infection leads to phosphorylation in a CSNK1A1-dependent manner (PubMed:29343571).
Ubiquitinated after phosphorylation in a CSNK1A1-dependent manner, leading to the lysosome-dependent degradation (PubMed:29343571). Proteasomally degraded through 'Lys-48'-mediated ubiquitination (PubMed:28883123). Ubiquitination is necessary for efficient IFNGR1 signaling (PubMed:28883123).

Chen, Q., Zhuang, S., Hong, Y., Yang, L., Guo, P., Mo, P., ... & Yu, C. (2022). Demethylase JMJD2D induces PD-L1 expression to promote colorectal cancer immune escape by enhancing IFNGR1-STAT3-IRF1 signaling. Oncogene, 41(10), 1421-1433.

Cheng, L., Zhang, F., Wang, Y., Chen, J., & Yuan, X. (2022). Association between IFNGR1 gene polymorphisms and tuberculosis susceptibility: A meta-analysis. Frontiers in Public Health, 10, 976221.

Du, W., Hua, F., Li, X., Zhang, J., Li, S., Wang, W., ... & Zou, W. (2021). Loss of optineurin drives cancer immune evasion via palmitoylation-dependent IFNGR1 lysosomal sorting and degradation. Cancer discovery, 11(7), 1826-1843.

Ortiz Fernandez, L., Coit, P., Yilmaz, V., Yentür, S. P., Alibaz‐Oner, F., Aksu, K., ... & Sawalha, A. H. (2021). Genetic Association of a Gain‐of‐Function IFNGR1 Polymorphism and the Intergenic Region LNCAROD/DKK1 With Behçet’s Disease. Arthritis & Rheumatology, 73(7), 1244-1252.

Singh, S., Kumar, S., Srivastava, R. K., Nandi, A., Thacker, G., Murali, H., ... & Chakrabarti, R. (2020). Loss of ELF5–FBXW7 stabilizes IFNGR1 to promote the growth and metastasis of triple-negative breast cancer through interferon-γ signalling. Nature cell biology, 22(5), 591-602.

Wang, Y., Niu, H., Liu, Y., Yang, H., Zhang, M., & Wang, L. (2020). Promoting effect of long non-coding RNA SNHG1 on osteogenic differentiation of fibroblastic cells from the posterior longitudinal ligament by the microRNA-320b/IFNGR1 network. Cell Cycle, 19(21), 2836-2850.

Wu, S., Liu, X., Wang, Y., Zhang, M., Wang, M., & He, J. Q. (2019). Genetic polymorphisms of IFNG and IFNGR1 with latent tuberculosis infection. Disease Markers, 2019.

Wu, S., Wang, Y., Zhang, M., Wang, M., & He, J. Q. (2019). Genetic variants in IFNG and IFNGR1 and tuberculosis susceptibility. Cytokine, 123, 154775.

Yoo, I., Seo, H., Choi, Y., Jang, H., Han, J., Lee, S., ... & Ka, H. (2019). Analysis of interferon‐γ receptor IFNGR1 and IFNGR2 expression and regulation at the maternal‐conceptus interface and the role of interferon‐γ on endometrial expression of interferon signaling molecules during early pregnancy in pigs. Molecular Reproduction and Development, 86(12), 1993-2004.

Khanolkar, A., Kirschmann, D. A., Caparelli, E. A., Wilks, J. D., Cerullo, J. M., Bergerson, J. R., ... & Fuleihan, R. L. (2018). CD4 T cell–restricted IL-2 signaling defect in a patient with a novel IFNGR1 deficiency. Journal of Allergy and Clinical Immunology, 141(1), 435-439.

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For research use only. Not intended for any clinical use.

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