InVivoMAb Anti-Human IFN-alpha/beta R1 Antibody (H3K1) (HB823010)

Name: InVivoMAb Anti-Human IFN-alpha/beta R1 Antibody (H3K1)
Brand: abinScience
SKU: HB823010
Price: 370 USD
Availability: InStock

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100ug
1mg

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Overview

Catalog No.	HB823010
Description	InVivoMAb Anti-Human IFNAR1 Antibody (H3K1) [H3K1] (HB823010) is a mouse monoclonal antibody detecting Interferon alpha/beta receptor 1 in Neutralization. Suitable for Human.
Species reactivity	Human
Applications	Neutralization
Host species	Mouse
Isotype	IgG2a, kappa
Clone ID	H3K1
Clonality	Monoclonal
Target	Interferon alpha/beta receptor 1, Cytokine receptor family 2 member 1, Cytokine receptor class-II member 1, CRF2-1, IFN-R-1, IFNAR1, IFNAR, IFN-alpha/beta receptor 1, Type I interferon receptor 1
Endotoxin level	Please contact with the lab for this information.
Purity	>95% as determined by SDS-PAGE.
Associated products	pH 7.4 Dilution Buffer
Purification	Protein A/G purified from cell culture supernatant.
Accession	P17181
Form	Liquid
Storage buffer	0.01M PBS pH 7.4 Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.
Stability and Storage	Use a manual defrost freezer and avoid repeated freeze thaw cycles. Store at 2 to 8°C for frequent use. Store at -20 to -80°C for twelve months from the date of receipt.
Background	Interferon alpha/beta receptor 1 (IFNAR1) is a ~63 kDa protein. Together with IFNAR2, forms the heterodimeric receptor for type I interferons (including interferons alpha, beta, epsilon, omega and kappa). 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. 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. The activated kinases phosphorylate specific tyrosine residues on the intracellular domains of IFNAR1 and IFNAR2, forming docking sites for the STAT transcription factors. STAT proteins are then phosphorylated by the JAKs, promoting their translocation into the nucleus to regulate expression of interferon-regulated genes. 1. Russell-Harde, D. et al. (1999) Biochemical and biophysical research communications 255, 539-44. PMID: 10049744 2. Kumar, KG. et al. (2003) The EMBO journal 22, 5480-90. PMID: 14532120 3. Kumar, KG. et al. (2004) The Journal of biological chemistry 279, 46614-20. PMID: 15337770 4. Uzé, G. et al. (1990) Cell 60, 225-34. PMID: 2153461 5. Thomas, C. et al. (2011) Cell 146, 621-32. PMID: 21854986 6. Zheng, H. et al. (2013) Cell reports 5, 180-93. PMID: 24075985 7. Hernandez, N. et al. (2019) The Journal of experimental medicine 216, 2057-2070. PMID: 31270247 8. Gothe, F. et al. (2022) Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 74, 136-139. PMID: 33252644 9. Bastard, P. et al. (2022) The Journal of experimental medicine 219. PMID: 35442418 10. Abramovich, C. et al. (1994) The EMBO journal 13, 5871-7. PMID: 7813427
Note	For research use only. Not suitable for clinical or therapeutic use.