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产品名称
起订量
单价(含增值税)
库存(PCS)
起订数量
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Recombinant Human SOD1/Cu-Zn SOD/Cu/Zn Superoxide48T-96T¥ 0.001
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Recombinant Human SOD1/Cu-Zn SOD/Cu/Zn SuperoxideGV-P01720-10ug¥ 1800.001
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Recombinant Human SOD1/Cu-Zn SOD/Cu/Zn SuperoxideGV-P01720-50ug¥ 4720.001
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Recombinant Human SOD1/Cu-Zn SOD/Cu/Zn SuperoxideGV-P01720-500ug¥ 13520.001
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Recombinant Human SOD1/Cu-Zn SOD/Cu/Zn SuperoxideGV-P01720-1mg¥ 18800.001
产品简介
Known as | Superoxide Dismutase [Cu-Zn]; Superoxide Dismutase 1; hSod1; SOD1 |
Derived from | E.coli |
Purity | Greater than 90% as determined by reducing SDS-PAGE. |
Formulation | Supplied as a 0.2 μm filtered solution of 20mM PB, 150mM NaCl, pH 7.2. |
Storage | Store at ≤-70°C, stable for 6 months after receipt.Store at ≤-70°C, stable for 3 months under sterile conditions after opening.Please minimize freeze-thaw cycles. |
Endotoxin | Less than 0.1 ng/ug (1 EU/ug) as determined by LAL test. |
Background | Superoxide Dismutase [Cu-Zn] (SOD1) is a soluble cytoplasmic and mitochondrial intermembrane space protein that belongs to the Cu-Zn superoxide dismutase family. SOD1 binds copper and zinc ions and is one of three isozymes responsible for destroying free superoxide radicals in the body. SOD1 neutralizes supercharged oxygen molecules, which can damage cells if their levels are not controlled. The enzyme protects the cell against dangerous levels of superoxide. Zinc binding promotes dimerization and stabilizes the native form. Mutations in SOD1 cause a form of familial amyotrophic lateral sclerosis. Defects in SOD1 are the cause of amyotrophic lateral sclerosis type 1 (ALS1) which is a familial form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper and lower motor neurons and resulting in fatal paralysis. |
规格 | 10ug50ug500ug1mg |
注意:
1.本产品仅供科研使用。请勿用于医药、临床诊断或治疗,食品及化妆品等用途。请勿存放于普通住宅区。
2.为了您的安全和健康,请穿好实验服并佩戴一次性手套和口罩操作。
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