SRP3061
IFN-omega human
recombinant, expressed in E. coli, ≥98% (SDS-PAGE), ≥98% (HPLC), suitable for cell culture
Synonym(s):
IFN alpha II-1, IFNW1, Interferon-alpha II-1, Interferon-omega
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About This Item
UNSPSC Code:
12352202
NACRES:
NA.32
biological source
human
recombinant
expressed in E. coli
Assay
≥98% (HPLC)
≥98% (SDS-PAGE)
form
lyophilized
potency
≤0.01 ng/mL ED50
mol wt
19.9 kDa
packaging
pkg of 100 μg
technique(s)
cell culture | mammalian: suitable
impurities
<0.1 EU/μg endotoxin, tested
color
white to off-white
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
Gene Information
human ... IFNW1(3467)
General description
IFN-ω is a type I interferon, which can be induced by virus-infected leukocytes. Members of the type I interferon family, which includes IFN-α, IFN-β, and IFN-ω, signal through IFNAR-1/IFNAR-2 receptor complex, and exert antiviral and antiproliferative activities. IFN-ω exhibits about 75% sequence homology with IFN- α, and contains two conserved disulfide bonds, which are necessary for full biological activity. Recombinant Human IFN-ω is a 19.9 kDa protein consisting of 173 amino acid residues.
Biochem/physiol Actions
IFN-ω is a type I interferon, which can be induced by virus-infected leukocytes. Members of the type I interferon family, which includes IFN-α, IFN-β, and IFN-ω, signal through IFNAR-1/IFNAR-2 receptor complex, and exert antiviral and antiproliferative activities. IFN-ω exhibits about 75% sequence homology with IFN- α, and contains two conserved disulfide bonds, which are necessary for full biological activity. Recombinant Human IFN-ω is a 19.9 kDa protein consisting of 173 amino acid residues.
Physical form
Lyophilized with no additives.
Preparation Note
Centrifuge the vial prior to opening. Reconstitute in water to a concentration of 1.0 mg/ml. Do not vortex. This solution can be stored at 2-8°C for up to 1 week. For extended storage, it is recommended to further dilute in a buffer containing a carrier protein (example 0.1% BSA) and store in working aliquots at -20°C to -80°C.
Other Notes
MCDLPQNHGL LSRNTLVLLH QMRRISPFLC LKDRRDFRFP QEMVKGSQLQ KAHVMSVLHE MLQQIFSLFH TERSSAAWNM TLLDQLHTGL HQQLQHLETC LLQVVGEGES AGAISSPALT LRRYFQGIRV YLKEKKYSDC AWEVVRMEIM KSLFLSTNMQ ERLRSKDRDL GSS
Storage Class Code
11 - Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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Hassan Abolhassani et al.
Journal of clinical immunology, 42(3), 471-483 (2022-01-30)
Inborn errors of immunity (IEI) and autoantibodies to type I interferons (IFNs) underlie critical COVID-19 pneumonia in at least 15% of the patients, while the causes of multisystem inflammatory syndrome in children (MIS-C) remain elusive. To detect causal genetic variants
Nikaïa Smith et al.
Nature communications, 13(1), 7254-7254 (2022-11-27)
Host immunity to infection with SARS-CoV-2 is highly variable, dictating diverse clinical outcomes ranging from asymptomatic to severe disease and death. We previously reported reduced type I interferon in severe COVID-19 patients preceded clinical worsening. Further studies identified genetic mutations
Hassan Abolhassani et al.
Journal of clinical immunology (2021-10-24)
Coronavirus disease 2019 (COVID-19) exhibits a wide spectrum of clinical manifestations, ranging from asymptomatic to critical conditions. Understanding the mechanism underlying life-threatening COVID-19 is instrumental for disease prevention and treatment in individuals with a high risk. We aimed to identify
Angelique Chauvineau-Grenier et al.
Research square (2021-10-07)
Recent studies reported the presence of pre-existing autoantibodies (auto-Abs) neutralizing type I interferons (IFNs) in at least 15% of patients with critical or severe COVID-19 pneumonia. In one study, these auto-Abs were found in almost 20% of deceased patients across
Romain Arrestier et al.
Annals of intensive care, 12(1), 121-121 (2023-01-01)
Auto-antibodies (auto-Abs) neutralizing type I interferons (IFN) have been found in about 15% of critical cases COVID-19 pneumonia and less than 1% of mild or asymptomatic cases. Determining whether auto-Abs influence presentation and outcome of critically ill COVID-19 patients could
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