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Merck
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重要文件

SRP5136

Sigma-Aldrich

SOD2, GST tagged human

recombinant, expressed in E. coli, ≥70% (SDS-PAGE), buffered aqueous glycerol solution

同義詞:

IPO-B, MNSOD, Mn-SOD

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About This Item

CAS號碼:
分類程式碼代碼:
12352200
NACRES:
NA.32

生物源

human

重組細胞

expressed in E. coli

化驗

≥70% (SDS-PAGE)

形狀

buffered aqueous glycerol solution

分子量

~51 kDa

NCBI登錄號

應用

cell analysis

運輸包裝

dry ice

儲存溫度

−70°C

基因資訊

human ... SOD2(6648)

一般說明

SOD2 (superoxide dismutase 2) is a member of the iron/manganese superoxide dismutase family. SOD2 binds to the superoxide byproducts of the mitochondrial electron transport chain and converts them to hydrogen peroxide and diatomic oxygen. Failure of SOD2 to remove the superoxide byproducts leads to an increase in mitochondrial reactive oxygen species resulting in biochemical aberrations with features reminiscent of mitochondrial myopathy, Friedreich ataxia, and HMGCL deficiency. Mutations in SOD2 have been associated with idiopathic cardiomyopathy (IDC), premature aging, sporadic motor neuron disease, and cancer.

外觀

Supplied in 50mM Tris-HCl, pH 7.5, 150mM NaCl, 10mM glutathione, 0.1mM EDTA, 0.25mM DTT, 0.1mM PMSF, 25% glycerol.

準備報告

after opening, aliquot into smaller quantities and store at -70 °C. Avoid repeating handling and multiple freeze/thaw cycles

儲存類別代碼

10 - Combustible liquids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable


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分析證明 (COA)

Lot/Batch Number

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S Melov et al.
Nature genetics, 18(2), 159-163 (1998-02-14)
Reactive oxygen species (ROS) have been implicated in a wide range of degenerative processes including amyotrophic lateral sclerosis, ischemic heart disease, Alzheimer disease, Parkinson disease and aging. ROS are generated by mitochondria as the toxic by-products of oxidative phosphorylation, their
S Hiroi et al.
Biochemical and biophysical research communications, 261(2), 332-339 (1999-07-30)
To reveal genetic risk factors of nonfamilial idiopathic cardiomyopathy (IDC) in Japanese, polymorphisms in the SOD2 and HLA-DRB1 genes were investigated in 86 patients and 380 healthy controls. There was a significant excess of homozygotes for the V allele [Val

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