Sample type Serum, Plasma, Cell Culture Supernatant, Other liquid samples
Components
Break apart microtiter test strips each coated single wells
8 x 12 (96 Total)
Lyophilized Standard
2 x vial
Biotin-labeled Antibody(Concentrated, 100X)
120 uL
HRP-Streptavidin Conjugate(Concentrated, 100X)
120 uL
Washing solution concentrate (25X)
30 mL
Sample Dilution buffer
20 mL
Antibody Dilution buffer
10 mL
Streptavidin Dilution buffer
10 mL
Stopping solution
10 mL
TMB Substrate (ready-to-use)
10 mL
Plate seals
3
Storage Store at 2-8°C.
target relevance
anti-Anifrolumab antibody Anti-drug antibodies (ADAs) generated in subjects following administration of Anifrolumab.
Anifrolumab Anifrolumab biologic drug binds Homo sapiens IFNAR1 Interferon alpha/beta receptor 1
Homo sapiens IFNAR1 Interferon alpha/beta receptor 1
Protein names Interferon alpha/beta receptor 1
Alternative names Cytokine receptor class-II member 1, Cytokine receptor family 2 member 1, Type I interferon receptor 1
Gene names IFNAR1
Protein family Belongs to the type II cytokine receptor family
Function Together with IFNAR2, forms the heterodimeric receptor for type I interferons (including interferons alpha, beta, epsilon, omega and kappa) (PubMed:10049744, PubMed:14532120, PubMed:15337770, PubMed:2153461, PubMed:21854986, PubMed:24075985, PubMed:31270247, PubMed:33252644, PubMed:35442418, PubMed:7813427). Type I interferon binding activates the JAK-STAT signaling cascade, resulting in transcriptional activation or repression of interferon-regulated genes that encode the effectors of the interferon response (PubMed:10049744, PubMed:21854986, PubMed:7665574). Mechanistically, type I interferon-binding brings the IFNAR1 and IFNAR2 subunits into close proximity with one another, driving their associated Janus kinases (JAKs) (TYK2 bound to IFNAR1 and JAK1 bound to IFNAR2) to cross-phosphorylate one another (PubMed:21854986, PubMed:32972995, PubMed:7665574, PubMed:7813427). The activated kinases phosphorylate specific tyrosine residues on the intracellular domains of IFNAR1 and IFNAR2, forming docking sites for the STAT transcription factors (PubMed:21854986, PubMed:32972995, PubMed:7526154, PubMed:7665574, PubMed:7813427). STAT proteins are then phosphorylated by the JAKs, promoting their translocation into the nucleus to regulate expression of interferon-regulated genes (PubMed:19561067, PubMed:21854986, PubMed:32972995, PubMed:7665574, PubMed:7813427, PubMed:9121453). Can also act independently of IFNAR2: form an active IFNB1 receptor by itself and activate a signaling cascade that does not involve activation of the JAK-STAT pathway (By similarity)
Subcellular location Cell membrane, Late endosome, Lysosome
Structure Heterodimer with IFNAR2; forming the receptor for type I interferon (PubMed:10049744, PubMed:21854986, PubMed:7665574). Interacts with TYK2 (PubMed:15337770, PubMed:24704786, PubMed:7526154). Interacts with STAT1 and STAT2; the interaction requires its phosphorylation at Tyr-466 (PubMed:9121453). Interacts (serine-phosphorylated form) with FBXW11, the substrate recognition component of a SCF (SKP1-CUL1-F-box protein) E3 ubiquitin-protein ligase complex (PubMed:14532120, PubMed:15337770, PubMed:18056411). Interacts with SHMT2; this promotes interaction with ABRAXAS2 and the BRISC complex (PubMed:24075985). Interacts with TRIM10; this interaction prevents association between IFNAR1 and TYK2 (PubMed:33811647)
Post-translational modification Ubiquitinated, leading to its internalization and degradation (PubMed:14532120, PubMed:15337770). Polyubiquitinated via 'Lys-48'-linked and 'Lys-63'-linked ubiquitin chains, leading to receptor internalization and lysosomal degradation (PubMed:18056411). The 'Lys-63'-linked ubiquitin chains are cleaved off by the BRISC complex (PubMed:24075985) Phosphorylated on tyrosine residues in response to interferon-binding: phosphorylation by TYK2 tyrosine kinase creates docking sites for STAT proteins (PubMed:10049744, PubMed:7526154). Phosphorylated on serine residues in response to interferon binding; this promotes interaction with FBXW11 and ubiquitination (PubMed:14532120, PubMed:15337770, PubMed:24075985) Palmitoylation at Cys-463 is required for the activation of STAT1 and STAT2
Involvement in disease Immunodeficiency 106, susceptibility to viral infections An autosomal recessive immunologic disorder characterized by increased susceptibility to viral infections beginning in infancy or early childhood. IMD106 affected individuals may demonstrate adverse reactions to vaccination with live attenuated viral vaccines, most notably measles, mumps and rubella (MMR) and yellow fever vaccines. A subset of IMD106 patients develop severe reactions, including excessive hyperinflammatory response, encephalopathy, acute respiratory distress syndrome, and multiorgan failure. IMD106 may also predispose to severe respiratory infection with SARS-CoV-2.
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Published literature highly relevant to the biological target of this product and referencing this antibody or clone are retrieved from the PubMed database provided by the United States National Library of Medicine at the National Institutes of Health.
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