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Key Documents

SRP3061

Sigma-Aldrich

IFN-omega human

recombinant, expressed in E. coli, ≥98% (SDS-PAGE), ≥98% (HPLC), suitable for cell culture

同義詞:

IFN alpha II-1, IFNW1, Interferon-alpha II-1, Interferon-omega

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About This Item

分類程式碼代碼:
12352202
NACRES:
NA.32

生物源

human

重組細胞

expressed in E. coli

化驗

≥98% (HPLC)
≥98% (SDS-PAGE)

形狀

lyophilized

效力

≤0.01 ng/mL ED50

分子量

19.9 kDa

包裝

pkg of 100 μg

技術

cell culture | mammalian: suitable

雜質

<0.1 EU/μg endotoxin, tested

顏色

white to off-white

UniProt登錄號

運輸包裝

wet ice

儲存溫度

−20°C

基因資訊

human ... IFNW1(3467)

一般說明

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.

生化/生理作用

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.

序列

MCDLPQNHGL LSRNTLVLLH QMRRISPFLC LKDRRDFRFP QEMVKGSQLQ KAHVMSVLHE MLQQIFSLFH TERSSAAWNM TLLDQLHTGL HQQLQHLETC LLQVVGEGES AGAISSPALT LRRYFQGIRV YLKEKKYSDC AWEVVRMEIM KSLFLSTNMQ ERLRSKDRDL GSS

外觀

Lyophilized with no additives.

重構

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.

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 3

閃點(°F)

Not applicable

閃點(°C)

Not applicable


分析證明 (COA)

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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
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
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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