Anti-Interferon-α Receptor, Type I, Subunit I (Ser535,539) Antibody
Our Anti-Interferon-α Receptor, Type I, Subunit I (Ser535,539) rabbit polyclonal phosphospecific primary antibody from PhosphoSolutions is produced in-house. It detects human Interferon-α Receptor, Type I, Subunit I (Ser535,539) and is antigen affinity purified from pooled serum. It is great for use in WB.
Western blot of immunoprecipitates from HEK 293 cells transfected with 1) Mock, 2) IFNAR1 WT, and 3) IFNAR1 S535A and S539A mutants. Specific immunolabeling of the ~110 kDa to ~130 kDa IFNAR1 WT (2) is shown in the first blot, as the immunolabeling is absent in IFNAR1 Ser535 and Ser539 mutants (3). The specific immunolabeling is blocked by the phosphopeptide (+) used as the antigen in the second blot.
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SKU: p170-5359
Ships: 1-2 business days
Product Details
Interferon-α Receptor, Type I, Subunit I (Ser535,539)
Interferons are widely used therapeutic agents because of their anti tumor and antiviral effects and because of their modulatory effects on the immune system (Biron, 2001; Kirkwood, 2002). These cytokines produce their effects by binding to the Type 1 Interferon-α Receptor (IFNAR1). Down regulation of this receptor plays a key role in determining the magnitude and duration of cytokine signaling. This down regulation is thought to be influenced by phosphorylation of Serine-535 and Ser-539 in the IFNAR1 (Kumar et al., 2003).
Antigen Affinity Purified from Pooled Serum
Polyclonal
IgG
ELISA, WB
Rabbit
IFNAR1
110-130 kDa
Synthetic phospho-peptide corresponding to amino acid residues surrounding Ser535/539 of human interferon-α, conjugated to keyhole limpet hemocyanin (KLH).
Human
Human
Bovine, Canine, Non-Human Primate, Mouse, Rat, Sheep
AB_2492138
Storage at -20°C is recommended, as aliquots may be taken without freeze/thawing due to presence of 50% glycerol. Stable for at least 1 year at -20°C.
Liquid
Prepared from pooled rabbit serum by affinity purification via sequential chromatography on phospho and non-phosphopeptide affinity columns.
10 mM HEPES (pH 7.5), 150 mM NaCl, 100 µg per ml BSA and 50% glycerol.
WB: 1:1000
Unconjugated
Specific for IFNAR1 protein phosphorylated at Ser535,539. Note: the molecular weight of the IFNAR1 varies with cell line (different levels of glycosylation) in 293 and HeLa Cells; the mature form is ~110 kDa - 130 kDa.
Phosphorylated
Ser535,539
Western blots performed on each lot.
For research use only. Not intended for therapeutic or diagnostic use. Use of all products is subject to our terms and conditions, which can be viewed on our website.
After date of receipt, stable for at least 1 year at -20°C.
AVP; Alpha-Type Antiviral Protein; IFNAR; Alpha; IFNBR; IFRC; interferon alpha/beta receptor 1; CRF2-1; IFN-R-1; IFN-alpha/beta receptor 1; beta-type antiviral protein; cytokine receptor class-II member 1; cytokine receptor family 2 member 1; interferon (alpha; beta and omega receptor 1; interferon receptor 1; interferon-alpha/beta receptor alpha chain; interferon-beta receptor 1; type I interferon receptor 1; IFN-Alpha-REC; Interferon Alpha And Beta Receptor Subunit 1; Interferon
P17181
UniProt Summary: 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). {ECO:0000250|UniProtKB:P33896, ECO:0000269|PubMed:10049744, ECO:0000269|PubMed:14532120, ECO:0000269|PubMed:15337770, ECO:0000269|PubMed:19561067, ECO:0000269|PubMed:2153461, ECO:0000269|PubMed:21854986, ECO:0000269|PubMed:24075985, ECO:0000269|PubMed:31270247, ECO:0000269|PubMed:32972995, ECO:0000269|PubMed:33252644, ECO:0000269|PubMed:35442418, ECO:0000269|PubMed:7526154, ECO:0000269|PubMed:7665574, ECO:0000269|PubMed:7813427, ECO:0000269|PubMed:9121453}.
UniProt Summary: 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). {ECO:0000250|UniProtKB:P33896, ECO:0000269|PubMed:10049744, ECO:0000269|PubMed:14532120, ECO:0000269|PubMed:15337770, ECO:0000269|PubMed:19561067, ECO:0000269|PubMed:2153461, ECO:0000269|PubMed:21854986, ECO:0000269|PubMed:24075985, ECO:0000269|PubMed:31270247, ECO:0000269|PubMed:32972995, ECO:0000269|PubMed:33252644, ECO:0000269|PubMed:35442418, ECO:0000269|PubMed:7526154, ECO:0000269|PubMed:7665574, ECO:0000269|PubMed:7813427, ECO:0000269|PubMed:9121453}.
3454
Blue Ice
- Western Blot Protocol: Download

