SOD1 cDNA ORF Clone, Mouse, N-His tag

Cat: MG52544-NH
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SOD1 cDNA ORF Clone, Mouse, N-His tag 基本信息
基因
种属
Mouse
NCBI 参考序列号
参考序列ORF长度
465 bp
描述
Full length Clone DNA of Mouse superoxide dismutase 1, soluble with N terminal His tag.
质粒
启动子
Enhanced CMV promoter
载体
pCMV3-N-His
标签序列
His Tag Sequence: CACCATCACCACCATCATCACCACCATCAC
测序引物
T7( 5' TAATACGACTCACTATAGGG 3' )
BGH( 5' TAGAAGGCACAGTCGAGG 3' )
质控
The plasmid is confirmed by full-length sequencing.
筛选
抗生素(大肠杆菌)
Kanamycin
抗生素(哺乳动物细胞)
Hygromycin
应用
Stable or Transient mammalian expression
储存 & 运输
运输
Each tube contains lyophilized plasmid.
储存
The lyophilized plasmid can be stored at ambient temperature for three months.

**Sino Biological guarantees 100% sequence accuracy of all synthetic DNA constructs we deliver, but we do not guarantee protein expression in your experimental system. Protein expression is influenced by many factors that may vary between experiments or laboratories.**

SOD1 cDNA ORF Clone, Mouse, N-His tag Alternative Names
B430204E11Rik cDNA ORF Clone, Mouse;Cu/Zn-SOD cDNA ORF Clone, Mouse;CuZnSOD cDNA ORF Clone, Mouse;Ipo-1 cDNA ORF Clone, Mouse;Ipo1 cDNA ORF Clone, Mouse;Sod-1 cDNA ORF Clone, Mouse;SODC cDNA ORF Clone, Mouse
SOD1 Background Information

SOD1 belongs to the Cu-Zn superoxide dismutase family. It binds copper and zinc ions and is one of two isozymes responsible for destroying free superoxide radicals in the body. The encoded isozyme is a soluble cytoplasmic protein, acting as a homodimer to convert naturally-occuring but harmful superoxide radicals to molecular oxygen and hydrogen peroxide. The other isozyme is a mitochondrial protein. Mutations in this gene have been implicated as causes of familial amyotrophic lateral sclerosis. Rare transcript variants have been reported for this gene. SOD1 destroys radicals which are normally produced within the cells and which are toxic to biological systems. Defects in SOD1 are the cause of amyotrophic lateral sclerosis type 1 (ALS1). ALS1 is a familial form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper and lower motor neurons and resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of cases leading to familial forms.

Full Name
superoxide dismutase 1, soluble
References
  • Murakami K, et al. (2011) SOD1 (copper/zinc superoxide dismutase) deficiency drives amyloid β protein oligomerization and memory loss in mouse model of Alzheimer disease. J Biol Chem. 286(52):44557-68.
  • Thompson M, et al. (2012) Paradoxical roles of serine racemase and D-serine in the G93A mSOD1 mouse model of amyotrophic lateral sclerosis. J Neurochem. 120(4):598-610.
  • Magrané J, et al. (2012) Mitochondrial dynamics and bioenergetic dysfunction is associated with synaptic alterations in mutant SOD1 motor neurons. J Neurosci. 32(1):229-42.
  • Gertz B, et al. (2012) Nuclear localization of human SOD1 and mutant SOD1-specific disruption of survival motor neuron protein complex in transgenic amyotrophic lateral sclerosis mice. J Neuropathol Exp Neurol. 71(2):162-77.
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