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SOD1 ELISA 试剂盒

This 人 SOD1 ELISA Kit is a Colorimetric ELISA Kit designed to quantify 人 SOD1.
产品编号 ABIN4986813
发货至: 中国

Quick Overview for SOD1 ELISA 试剂盒 (ABIN4986813)

抗原

See all SOD1 ELISA试剂盒
SOD1 (Superoxide Dismutase 1, Soluble (SOD1))

适用

  • 7
  • 3
  • 3
  • 2
  • 2
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1

检测方法

Colorimetric

实验类型

Sandwich ELISA

检测范围

78-5000 pg/mL

应用范围

ELISA

样品类型

Cell Culture Supernatant, Serum, Plasma (heparin), Plasma (citrate), Plasma (EDTA)
  • 最低检测浓度

    78 pg/mL

    Analytical Method

    Quantitative

    特异性

    Natural and recombinant Human Cu/ZnSOD Ligand

    灵敏度

    40 pg/mL

    试剂未包括

    • Microplate reader.
    • Pipettes and pipette tips.
    • EP tube Deionized or distilled water.
  • 应用备注

    Detection Wavelength: 450 nm

    样本量

    20 μL

    实验时间

    3 h

    板类型

    Pre-coated

    限制

    仅限研究用
  • 储存条件

    4 °C
  • 抗原 See all SOD1 ELISA试剂盒

    SOD1 (Superoxide Dismutase 1, Soluble (SOD1))

    别名

    Cu/ZnSOD

    背景

    Superoxide Dismutases (SODs), originally identified as Indophenoloxidase (IPO), are enzymes that catalyze the conversion of naturallyoccuring but harmful superoxide radicals into molecular oxygen and hydrogen peroxide. Superoxide Dismutases 1, SOD1, also known as Cu/Zn SOD, soluble SOD and IPOA, is a soluble, cytoplasmic 16 kDa homodimer. Each SOD1 monomer binds one Cu2+ and one Zn2+ ion. Three isozymes of SOD have been identified and are functionally related but have very modest sequence homology. SOD1 shares 23 % and 27 % sequence identity with SOD2 and SOD3, respectively. Mutations in SOD1 have been implicated as causes of familial amyotrophic lateral sclerosis (ALS). The ALScausing mutations of SOD1 are scattered throughout the protein and provide no clear functional or structural clues to the underlying disease mechanism. The oligomerization hypothesis suggests that mutant SOD1 proteins become misfolded and consequently oligomerize into high molecular weight aggregates that result in the death of motor neurons. The oxidative damage hypothesis suggests that loss of function mutation in SOD1 protein results in the accumulation of cellular superoxide radical, leading to free radicalmediated damage, the release of cytochrome c, and apoptosis.

    途径

    Sensory Perception of Sound, Transition Metal Ion Homeostasis
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