SRP3061
IFN-omega human
recombinant, expressed in E. coli, ≥98% (SDS-PAGE), ≥98% (HPLC), suitable for cell culture
Sinónimos:
IFN alpha II-1, IFNW1, Interferon-alpha II-1, Interferon-omega
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About This Item
UNSPSC Code:
12352202
NACRES:
NA.32
Productos recomendados
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)
Categorías relacionadas
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.
Sequence
MCDLPQNHGL LSRNTLVLLH QMRRISPFLC LKDRRDFRFP QEMVKGSQLQ KAHVMSVLHE MLQQIFSLFH TERSSAAWNM TLLDQLHTGL HQQLQHLETC LLQVVGEGES AGAISSPALT LRRYFQGIRV YLKEKKYSDC AWEVVRMEIM KSLFLSTNMQ ERLRSKDRDL GSS
Physical form
Lyophilized with no additives.
Reconstitution
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.
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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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
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
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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
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
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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